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Physiology of pain

  • Pain is an unpleasant sensory and emotional experience
  • Associated with potential or actual tissue damage
  • It is a complex interaction of
    • Sensory factors
    • Emotional factors
    • Behavioural factors
  • Stimuli activate the nociceptive system
  • Conveyed to brain by an adaptable pathway
  • Pain is only experienced in the conscious brain

Somatic pain

First pain

  • First or 'fast' pain is a protective response
  • Allows rapid withdrawal from a painful stimulus
  • Due to stimulation of high threshold thermo / mechanical receptors
  • Transmitted by fast myelinated A fibres
  • Enter dorsal horn of spinal cord
  • Secondary fibres in spinothalamic tract transmit stimulus to posterior thalamic nuclei
  • Tertiary fibres transmit stimulus to somatosensory post-central gyrus

Secondary pain

  • Secondary or 'slow' pain is responsible for delayed sensation of pain
  • Elicits behaviour to protect damaged tissue
  • Initiates reflex responses to pain such as tachycardia, hypertension and increased respirator rate
  • Due to stimulation of high threshold polymodal receptors
  • Respond to mechanical, thermal and chemical stimuli
  • Transmitted by slow unmyelinated C fibres
  • Enter dorsal horn
  • Secondary fibres in palaeospinothalamic tract transmits stimulus to medial thalamic nuclei
  • Collateral transmit to midbrain, medullary reticular formation and hypothalamus
  • Further information is transmitted to forebrain limbic system

Visceral pain

  • Fewer visceral nociceptors than somatic receptors
  • Cortical mapping is less concentrated
  • Visceral pain is poorly localised
  • Pain is also qualitatively different due to progressive stimulation and summation
  • May also be referred to site away from source of stimulation

Physiology

Peripheral activation

  • Most pain originates after tissue damage
  • Due to the local release of inflammatory mediators
  • Mediators involved include:
    • Leukotrienes D4 and B4
    • Bradykinin
    • Histamine
    • 5HT
  • Activate or sensitise high threshold nociceptors
  • Results in primary hyperalgesia

Spinal level

  • Occurs in dorsal horn of spinal cord
  • Complex interaction between excitatory and inhibitory interneurons
  • Also involves descending inhibitory tracts in spinal cord
  • Gate Control Theory explains non-linear relation injury and response
  • Suggests that pain can be 'gated-out' in dorsal horn by other stimuli
  • Neurotransmitters involved are:
    • Excitatory amino acids
    • Neuropeptides
  • Some neuropeptides increase nociception - Substance P,  bombesin, VIP
  • Other neuropeptides reduce nociception - galanin, somatostatin, GABA

Supraspinal level

  • Perception of pain is associated with activity in:
    • Thalamus
    • Primary and secondary cortex
  • Various regions are involved with descending inhibition
  • Originate at level of cortex and thalamus
  • Mediated via relays in brainstem and dorsal columns to dorsal horns
  • Mediators involved:
    • Noradrenaline
    • 5HT
    • Endogenous opioids

 

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