Hyperalgesia (+ Central Sensitisation)

• Hyperalgesia:

  • at the injured tissues theres an area sensitive to thermal and mechanical stimuli - primary hyperalgesia
  • primary hyperalgesia is due to peripheral nerve sensitisation
  • a wider area of sensitivity is found surrounding the injury (only sensitive to mechanical stimuli) - secondary hyperalgesia
  • secondary hyperalgesia is due to sensitisation of dorsal horn cells (or above) - central sensitisation

  A) primary hyperalgesia

  B) secondary hyperalgesia

  
• Central Sensitisation pt 1:

  • regarding the pain gate, various influences can impact the excitability of dorsal horn cell (DHC) (how ready it is to fire) to fire nociceptive information up to the brain, where we'd be more likely to feel pain
  • when we have a injured tissue causing inflammation or a nerve injury, causing ectopic firing of a nerve, we get ongoing excitatory nociceptive input (afferent barrage) to DHC - this causes changes to the function and properties of the DHC which shows the DHC is becoming sensitised and lowering its threshold to fire, so becoming more excitable
• Central Sensitisation pt 2:

  • in a sensitised dorsal horn cell there will be an amplified response to afferent input, causing exaggerated pain to a normal level of nociceptive input
  • there will also be a reduction in threshold for firing of the dorsal horn cell, so it would fire to stimuli that previously wouldnt have made it fire - non noxious input is now painful
  • there might also be expansion of the receptive field of the dorsal horn cell, causing the spreading of pain and tenderness, as the excitability of the dorsal horn cell spreads pain wider than the area of actual tissue damage