Flashcards in An Introduction to Pain and Thermosensation Deck (21):
what are the three main types of pain?
nociceptive pain - immediate protective response, short lived
inflammatory pain - assists in healing, persists over days, possibly weeks
pathological pain - no physiological purpose, persists over months to years
describe the difference in sensation of cutaneous, muscular and visceral pain?
skin = well localised, pricking/stabbing
muscle = poorly localised, aching, tender, cramp
viscera = poorly localised (referred to a somatic structure), dull, vague, associated with nausea
what potential stimuli can activate nociceptors?
nociceptors are 1st order neurones - true or false?
true - relay info to second order neurones in CNS
what type of nerve fibres are nociceptors?
Aδ and C fibres
explain the difference in pain response from Aδ and C fibres?
Aδ = respond to noxious mechanical and thermal stimuli - not chemical - mediates first or "fast" pain
C = respond to all noxious stimuli (eg polymodal), mediate second or slow pain as they wait for inflammatory mediators to activate them
describe the difference in sensation between first "fast" pain from Aδ fibres and slow pain from C fibres?
first pain = stabbing, pricking sensation
second pain = burning, throbbing, cramping, aching sensations
what receptors can pick up noxious thermal stimuli?
members of the transient receptor potential (TRP) family = TRPA1, TRPC3 and TRPV1
TPRV1 is also active at normal body temp but when inflammation is present
what receptors do noxious chemical stimuli activate?
H+ = acid sensing ion channels (ASICs)
ATP = P2X and P2Y receptors
bradykinin = B2 receptors
what temperatures activate Aδ type I fibres?
Aδ type I = 53 degrees
Aδ type II or C = 43
what do efferent signals to nociceptor nerve endings cause?
release of pro-inflammatory mediators - calcitonin gene related peptide (CGRP) and substance P
these mediators contribute to neurogenic inflammation
what can noxious stimulation cause in the long term?
increases spinal excitability
more efferent signals causing pro-inflammatory mediators at peripheral nerve terminal
- can cause hyperalgesia (amplified pain) and allodynia (pain without noxious input)
explain the synaptic connection between the 1st and 2nd order neurone in nociception?
AP opens voltage-gated Ca2+ channels
glutamate releases from vesicles
activation of glutamate receptors
membrane depolarisation (e.p.s.p) - Mg2+ moves out of way in NDMA receptors
opening of voltage gated Na+ channels
where in the dorsal horn of the spinal cord do Aδ and C fibres terminate?
laminae of rexed I and II
laminae I contains nociceptive specific (NS) cells which synapse only with C- and Aδ fibres
then go on to interact with WDR neurone
what other type of nerve fibre (aside from Aδ and C) terminates in the laminae of rexed and has input to the wide dynamic range (WDR) neuron?
Aβ - proprioceptive
where does visceral pain come from?
coverings of organs eg pleura / peritoneum
when these are stretched / twisted / ischaemic = pain
no pain if cut / burnt
what nerve pathways are followed by visceral afferents from nociceptors before entering the dorsal horn of spinal cord?
follows sympathetic pathways
what is viscerosomatic pain and how does it present?
sharp and well localised pain
occurs when inflammatory exudate from diseased organ contacts body wall structure
may present with diffuse visceral pain that progresses to sharp viscerosomatic pain (eg appendicitis)
pain evoked by activity in nociceptors (C and Aδ- fibres) can be reduced by activity in Aβ fibres - true or false?
true - this details the gate control theory
patient often finds that focussing in low threshold activity involving Aβ fibres distracts them from pain
what is gate control theory?
firing of Aβ > Aδ and C fibres = gate closed
firing of Aβ < Aδ and C fibres = gate open
if gate is closed then no 2nd order nociceptive signals fire to the brain