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pain physiology Y2S1 2014

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pain physiology Y2S1 2014

  1. 1. Physiology of pain Prof. Vajira Weerasinghe Professor of Physiology, Faculty of Medicine, University of Peradeniya & Consultant Neurophysiologist, Teaching Hospital, Peradeniya www.slideshare.net/vajira54
  2. 2. Topics covered in the lecture 1. What is pain? (International definition of pain) 2. Dual nature of pain: fast pain and slow pain 3. What causes pain : pain stimuli 4. Nerve pathways carrying pain signals to the brain 5. Brain areas involved in pain perception 6. Pain modulatory pathways 7. Neurochemicals involved in pain pathways
  3. 3. What is pain? • Pain is a difficult word to define • Patients use different words to describe pain • eg. • 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 • Different words in Sinhala or in Tamil
  4. 4. What is pain? • There is an International definition of pain formulated by the IASP (International Association for the study of 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 2011
  5. 5. What is pain? • Pain is – subjective – protective – and it is modified by developmental, behavioural, personality and cultural factors • It is a symptom • Associated signs are crying, sweating, increased heart rate, blood pressure, behavioural changes etc
  6. 6. Measurement of pain • It is difficult to describe pain although we know what it is • It is difficult to measure pain – visual analogue scale (VAS) is used
  7. 7. Dual nature of pain • Fast pain – acute – pricking type – well localised – short duration – Thin myelinated nerve fibres are involved (A delta) • Slow pain – chronic – throbbing type – poorly localised – long duration – Unmyelinated nerve fibres are involved (c fibres)
  8. 8. Different situations •No stimuli, but pain is felt •phantom limb pain •eg. in amputated limb •Stimuli present, but no pain felt •eg. soldier in battle field, sportsman in arena •Pain due to a stimulus that does not normally provoke pain •Allodynia •Pain caused by a lesion or disease of the somatosensory nervous system •Neuropathic pain
  9. 9. Pain terminology International Association for the Study of Pain 2011 • Hyperalgesia – Increased pain from a stimulus that normally provokes pain • Hyperaesthesia – Increased sensitivity to stimulation, excluding the special senses (increased cutaneous sensibility to thermal sensation without pain ) • Paraesthesia – An abnormal sensation, whether spontaneous or evoked • Anaesthesia – A loss of sensation resulting from pharmacologic depression of nerve function or from neurological dysfunction • Neuralgia – Pain in the distribution of a nerve or nerves • Analgesia – Absence of pain in response to a normally painful stimulus • Allodynia – Pain due to a stimulus that does not normally provoke pain
  10. 10. Pain terminology International Association for the Study of Pain 2011 • Neuropathic Pain – Pain caused by a lesion or disease of the somatosensory nervous system • Nociceptive pain – Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors • Visceral pain – Pain arising from visceral organs (e.g., heart, lungs, gastrointestinal tract, liver, gallbladder, kidneys, bladder). • Neuropathy – A disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy • Nociception – The neural process of encoding noxious stimuli • Noxious stimulus – A stimulus that is damaging or threatens damage to normal tissues.
  11. 11. Pain • Pain as a sensation – physiologically (nociception) – Nociceptive pain • Pain as an emotional experience – Psychologically – Psychogenic pain • Pain caused by damage to nerve – Neuropathic pain
  12. 12. Transduction and perception • Transduction – Process of converting noxious stimulus to action potentials • Perception – Central processing of nociceptive impulses in order to interpret pain
  13. 13. Stimuli • Physical – pressure etc • Electrical • Thermal – cold, hot • Chemical – H+, lactic acid, K+, histamine, bradykinin, serotonin, leucotrines, acetylcholine, proteolytic enzymes, capsiacin – Prostaglandins (PGE2) • Cannot directly stimulate nociceptors • Increase the sensitivity of nociceptors for other stimuli (decrease the threshold)
  14. 14. Receptors  There are no specialised receptors  Pain receptors are called nociceptors  A sensory receptor that is capable of transducing and encoding noxious stimuli (actually or potentially tissue damaging stimuli)  Nociceptors are free nerve endings  Free nerve endings are distributed everywhere  both somatic and visceral tissues  except brain tissue and lung parenchyma
  15. 15. Receptors • Nociceptors are very slowly adapting type • Different types of nociceptors – Some respond to one stimulus – Some respond to many stimuli (polymodal) – Some may not respond to the standard stimuli (silent nociceptors) • they respond only when inflammatory substances are present • Capsaicin receptor (TRPV1 receptor) – Respond to capsaicin, heat, low pH – Stimulation leads to painful, burning sensation
  16. 16. Nerve pathways carrying pain signals to the brain • Pain signals enter the spinal cord • First synapse is present in the dorsal horn of the spinal cord • Then the second order neuron travels through the lateral spinothalamic tracts
  17. 17. afferent fibres • two types – Aδ (thin myelinated) – C (unmyelinated)
  18. 18. central connections • afferent fibre enters the spinal cord • synapses in laminae ii,iii – substantia gelatinosa substantia gelatinosa Neurotransmitter at the first synapse of the pain pathway is substance P • Acute pain : glutamate • Chronic pain: substance P • Pain inhibitory neurotransmitters: enkephalin, GABA
  19. 19. Pain lateral spinothalamic tract C fibre substantia gelatinosa • crosses the midline • ascends up as the lateral spinothalamic tract ascending pathway
  20. 20. lateral spinothalamic tract thalamus sensorycortex C fibre thalamo cortical tracts
  21. 21. Pain perception • This occurs at different levels – thalamus is an important centre of pain perception • lesions of thalamus produces severe type of pain known as ‘thalamic pain’ – Sensory cortex is necessary for the localisation of pain – Other areas are also important • reticular formation, limbic areas, hypothalamus and other subcortical areas
  22. 22. Pathophysiology of pain • Pain sensations could arise due to – Inflammation of the nerves (neuritis) – Injury to the nerves and nerve endings with scar formation (disk prolapse) – Injury to the structures in the spinal cord, thalamus or cortical areas that process pain information (spinal trauma) – Abnormal activity in the nerve circuits that is perceived as pain (phantom limb pain) – Nerve invasion, for example by cancer (brachial plexopathy)
  23. 23. Descending pain modulatory system • several lines of experimental evidence show the presence of descending pain modulatory system – stimulus produced analgesia (Reynolds) – stimulation of certain areas in the brain stem was known to decrease the neuronal transmission along the spinothalamic tract – discovery of morphine receptors – they were known to be present in the brain stem areas – discovery of endogenous opioid peptides • eg. Endorphines, enkephalins, dynorphin
  24. 24. midbrain pons medulla spinal cord periaqueductal grey nucleus nucleus raphe magnus substantia gelatinosa
  25. 25. opioid peptides • short peptides originally known to be secreted in CNS and later found to be present in GIT etc
  26. 26. opioid peptides ∀β endorphin • Earliest to discover, present in pituitary • encephalins - met & leu • widely distributed • dynorphin • Endomorphine 1 & 2 • Pronociceptins Receptors: mu, kappa, delta, recently discovered ORL1 receptor
  27. 27. • descending tracts involving opioid peptides as neurotransmitter were discovered • these were known to modify (inhibit) pain impulse transmission at the first synapse at the substantia gelatinosa
  28. 28. • first tract was discovered in 1981 by Fields and Basbaum – it involves enkephalin secreting neurons in the reticular formation – starting from the PAG (periaqueductal grey area) of the midbrain – ending in the NRM (nucleus raphe magnus) of the medulla – from their ending in the substantia gelatinosa of the dorsal horn
  29. 29. • in the subtantia gelatinosa – enkephalin secreting neuron is involved in presynaptic inhibition of the pain impulse transmission by blocking substance P release
  30. 30. substantia gelatinosa c fibre input descending inhibitory tract dorsal horn substantia gelatinosa cell
  31. 31. substance P enkephalin Presynaptic inhibition
  32. 32. Presynaptic inhibition substance P enkephalin pain impulse blocking of pain impulse
  33. 33. • since then various other descending tracts were discovered • all of them share following common features – involved in brain stem reticular areas – enkephalins act as neurotransmitters at least in some synapses – most of these tracts are inhibitory – midbrain nuclei are receiving inputs from various areas in the cortex, subcortical areas, limbic system, hypothalamus etc – the ascending tract gives feedback input to the descending tracts – recently even nonopioid peptides are known to be involved
  34. 34. sensorycortex C fibre Final pain perception depends on activity of the Ascending pain impulse transmitting tracts Descending pain modulatory (inhibitory) tracts
  35. 35. Theories of pain There is a single pathway for touch and pain Less intensity produces touch Increased intensity produces pain There are two different pathways for touch and pain Specificity theory touch pain Intensity theory touch pain
  36. 36. Gate control theory • This explains how pain can be relieved very quickly by a neural mechanism • First described by P.D. Wall & 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’
  37. 37. Gate control theory When pain fibre is stimulated, gate will be opened & pain is felt pain pain is felt + gate is opened
  38. 38. 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
  39. 39. 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 ?
  40. 40. Gate control theory • But the anatomcal basis for all the connections of Wall’s original diagram is lacking ? ?
  41. 41. WDR (wide dynamic range cells) • It is known that some of the second order neurons of the pain pathway behave as wide dynamic range neurons • They are responsive to several somatosensory modalities (thermal, chemical and mechanical) • They can be stimulated by pain but inhibited by touch stimuli
  42. 42. WDR (wide dynamic range cells) C fibre A fibre pain & mech mech inhibitory excitatory WDR cell
  43. 43. WDR cells • have been found in – Spinal cord – Trigeminal nucleus – Brain stem – Thalamus – Cortex
  44. 44. Modifications to the gate control theory • this could be modified in the light of enkephalin activity and WDR cells • inhibitory interneuron may be substantia gelatinosa cell • descending control is more important • WDR cells may represent neurons having pain as well as touch input
  45. 45. referred pain • sometimes pain arising from viscera are not felt at the site of origin but referred to a distant site. – eg. • cardiac pain referred to the left arm • diaphargmatic pain referred to the shoulder – this paradoxical situation is due to an apparent error in localisation
  46. 46. referred pain - theories • convergence theory – somatic & visceral structures converge on the same dermatome – generally impulses through visceral pathway is rare – centrally brain is programmed to receive impulses through somatic tract only – therefore even if the visceral structure is stimulated brain misinterpret as if impulses are coming from the somatic structure visceral somatic second order neuron ++ ++ + + +
  47. 47. referred pain - theories • facilitatory theory – somatic & visceral structures converge on the same dermatome – stimulation of visceral structure facilitates transmission through somatic tract visceral somatic second order neuron ++ ++ + + +
  48. 48. Pain memory • Memory of pain often overshadows its primary experience in its impact upon pathophysiology and human suffering • The memory of pain can be more damaging than its initial experience • Central sensitization – Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input • Peripheral sensitization – Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields • Clinical interventions to blunt both the experience and persistence of pain or to lessen its memory are now applied
  49. 49. Summary • Pain is not just a sensation but is a more complex phenomenon • Pain can be blocked at many places • Chemicals play an important role in causing pain as well as in reducing pain • Neural mechanisms also play a role in pain interaction • This complex nature of pain perception makes it a very difficult entity to control
  50. 50. “Pain is a more terrible lord of mankind than even death itself” Dr. Albert Schweitzer (1875-1965)

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