Y2 s1 pain physiology


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Y2 s1 pain physiology

  1. 1. Physiology of pain Prof. Vajira Weerasinghe Professor in Physiology, Faculty of Medicine University of Peradeniya & Consultant Neurophysiologist, Teaching Hospital, Peradeniya
  2. 2. Topics covered in the lecture <ul><li>What is pain (International definition of pain) </li></ul><ul><li>Dual nature of pain: fast pain and slow pain </li></ul><ul><li>What causes pain : pain stimuli </li></ul><ul><li>Nerve pathways carrying pain signals to the brain </li></ul><ul><li>Brain areas involved in pain perception </li></ul><ul><li>Pain modulatory pathways </li></ul><ul><li>Neurochemicals involved in pain pathways </li></ul><ul><li>Gate control theory of pain </li></ul>
  3. 3. What is pain? <ul><li>Pain is a difficult word to define </li></ul><ul><li>Patients use different words to describe pain </li></ul><ul><li>eg. </li></ul><ul><li>Aching, Pins and needles, Annoying, Pricking, Biting, Hurting, Radiating, Blunt, Intermittent, Burning, Sore, Miserable, Splitting, Cutting, Nagging, Stabbing, Crawling, Stinging, Crushing, Tender, Dragging, Numbness, Throbbing, Dull, Overwhelming, Tingling, Electric-shock like, Penetrating, Tiring, Excruciating, Piercing, Unbearable </li></ul><ul><li>Different words in Sinhala or in Tamil </li></ul>
  4. 4. What is pain? <ul><li>There is an International definition of pain formulated by the IASP (International Association for the study of pain) </li></ul><ul><li>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 </li></ul>
  5. 5. What is pain? <ul><li>Pain is </li></ul><ul><ul><li>subjective </li></ul></ul><ul><ul><li>protective </li></ul></ul><ul><ul><li>and it is modified by developmental, behavioural, personality and cultural factors </li></ul></ul><ul><li>It is a symptom </li></ul><ul><li>Associated signs are crying, sweating, increased heart rate, blood pressure, behavioural changes etc </li></ul>
  6. 6. Dual nature of pain <ul><li>Fast pain </li></ul><ul><ul><li>acute </li></ul></ul><ul><ul><li>pricking type </li></ul></ul><ul><ul><li>well localised </li></ul></ul><ul><ul><li>short duration </li></ul></ul><ul><ul><li>Thin myelinated nerve fibres are involved (A delta) </li></ul></ul><ul><li>Slow pain </li></ul><ul><ul><li>chronic </li></ul></ul><ul><ul><li>throbbing type </li></ul></ul><ul><ul><li>poorly localised </li></ul></ul><ul><ul><li>long duration </li></ul></ul><ul><ul><li>Unmyelinated nerve fibres are involved (c fibres) </li></ul></ul>
  7. 7. <ul><li>No stimuli, but pain is felt </li></ul><ul><ul><li>phantom limb pain </li></ul></ul><ul><ul><ul><li>eg. in amputated limb </li></ul></ul></ul><ul><li>Stimuli present, but no pain felt </li></ul><ul><ul><ul><li>eg. soldier in battle field, sportsman in arena </li></ul></ul></ul><ul><li>Pain due to a stimulus which does not normally provoke pain </li></ul><ul><ul><ul><li>Allodynia </li></ul></ul></ul><ul><li>Pain initiated or caused by a primary lesion or dysfunction in the nervous system </li></ul><ul><ul><ul><li>Neuropathic pain </li></ul></ul></ul>Different situations
  8. 8. Pain <ul><li>Pain as a sensation </li></ul><ul><ul><li>physiologically (nociception) </li></ul></ul><ul><li>Pain as an emotional experience </li></ul><ul><ul><li>psychologically </li></ul></ul>
  9. 9. Stimuli <ul><li>Physical </li></ul><ul><ul><li>pressure etc </li></ul></ul><ul><li>Electrical </li></ul><ul><li>Thermal </li></ul><ul><ul><li>cold, hot </li></ul></ul><ul><li>Chemical </li></ul><ul><ul><li>H+, lactic acid, K+, histamine, bradykinin, acetylcholine, proteolytic enzymes </li></ul></ul><ul><ul><li>Prostaglandins </li></ul></ul><ul><ul><ul><li>these increase the sensitivity (decrease the threshold) for other nociceptive stimuli </li></ul></ul></ul>
  10. 10. Receptors <ul><li>There are no specialised receptors </li></ul><ul><li>Free nerve endings are sensitive to pain stimuli </li></ul><ul><li>Free nerve endings are distributed everywhere (both somatic and visceral tissues) </li></ul><ul><li>Slow adapting type of receptors </li></ul>
  11. 11. Nerve pathways carrying pain signals to the brain <ul><li>Pain signals enter the spinal cord </li></ul><ul><li>First synapse is present in the dorsal horn of the spinal cord </li></ul><ul><li>Then the second order neuron travels through the lateral spinothalamic tracts </li></ul>
  12. 12. afferent fibres <ul><li>two types </li></ul><ul><ul><li>A  (thin myelinated) </li></ul></ul><ul><ul><li>C (unmyelinated) </li></ul></ul>
  13. 13. central connections <ul><li>afferent fibre enters the spinal cord </li></ul><ul><li>synapses in laminae ii,iii </li></ul><ul><ul><li>substantia gelatinosa </li></ul></ul>substantia gelatinosa Neurotransmitter at the first synapse of the pain pathway is substance P
  14. 14. <ul><li>crosses the midline </li></ul><ul><li>ascends up as the lateral spinothalamic tract </li></ul>ascending pathway Pain lateral spinothalamic tract C fibre substantia gelatinosa
  15. 15. lateral spinothalamic tract thalamus sensory cortex C fibre thalamocortical tracts
  16. 16. Pain perception <ul><li>This occurs at different levels </li></ul><ul><ul><li>thalamus is an important centre of pain perception </li></ul></ul><ul><ul><ul><li>lesions of thalamus produces severe type of pain known as ‘thalamic pain’ </li></ul></ul></ul><ul><ul><li>Sensory cortex is necessary for the localisation of pain </li></ul></ul><ul><ul><li>Other areas are also important </li></ul></ul><ul><ul><ul><li>reticular formation, limbic areas, hypothalamus and other subcortical areas </li></ul></ul></ul>
  17. 17. Descending pain modulatory system <ul><li>several lines of experimental evidence show the presence of descending pain modulatory system </li></ul><ul><ul><li>discovery of morphine receptors </li></ul></ul><ul><ul><ul><ul><li>they were known to be present in the brain stem areas </li></ul></ul></ul></ul><ul><ul><li>discovery of endogenous opioid peptides </li></ul></ul><ul><ul><ul><li>eg. Endorphines, enkephalins, dynorphin </li></ul></ul></ul>
  18. 18. midbrain pons medulla spinal cord periaqueductal grey nucleus nucleus raphe magnus substantia gelatinosa
  19. 19. opioid peptides <ul><li>short peptides originally known to be secreted in CNS and later found to be present in GIT etc </li></ul>
  20. 20. opioid peptides <ul><li> endorphin </li></ul><ul><ul><ul><li>earliest to discover, large peptide, present in the pituitary </li></ul></ul></ul><ul><li>encephalins - met & leu </li></ul><ul><ul><ul><li>widely distributed </li></ul></ul></ul><ul><li>dynorphin </li></ul><ul><li>Endomorphine 1 & 2 </li></ul><ul><li>Pronociceptins </li></ul>
  21. 21. receptors <ul><li>delta </li></ul><ul><li>mu </li></ul><ul><li>kappa </li></ul><ul><li>More recently discovered: ORL1 receptor </li></ul>
  22. 22. <ul><li>Final pain perception depends on activity of the </li></ul><ul><ul><li>Ascending pain impulse transmitting tracts </li></ul></ul><ul><ul><li>Descending pain modulatory (inhibitory) tracts </li></ul></ul>sensory cortex C fibre
  23. 23. Gate control theory <ul><li>This explains how pain can be relieved very quickly by a neural mechanism </li></ul><ul><li>First described by P.D. Wall & Melzack (1965) </li></ul><ul><li>“ There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a ‘ gating mechanism ’ </li></ul>
  24. 24. Gate control theory When pain fibre is stimulated, gate will be opened & pain is felt pain pain is felt + gate is opened
  25. 25. Gate control theory When pain and touch fibres are stimulated together, gate will be closed & pain is not felt pain is not felt touch pain + - gate is closed
  26. 27. Gate control theory <ul><li>This theory provided basis for various methods of pain relief </li></ul><ul><ul><li>Massaging a painful area </li></ul></ul><ul><ul><li>Applying irritable substances to a painful area (counter-irritation) </li></ul></ul><ul><ul><li>Transcutaneous Electrical Nerve Stimulation (TENS) </li></ul></ul><ul><ul><li>Acupuncture ? </li></ul></ul>
  27. 28. Summary <ul><li>Pain is not just a sensation but is a more complex phenomenon </li></ul><ul><li>Pain can be blocked at many places </li></ul><ul><li>Chemicals play an important role in causing pain as well as in reducing pain </li></ul><ul><li>Neural mechanisms also play a role in pain interaction </li></ul><ul><li>This complex nature of pain perception makes it a very difficult entity to control </li></ul>
  28. 29. <ul><li>“ Pain is a more terrible lord of mankind than even death itself” </li></ul><ul><li>Dr. Albert Schweitzer (1875-1965) </li></ul>