An Introduction to Pain and Thermosensation

Question 1

what are the three main types of pain?

Answer 1

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

Question 2

describe the difference in sensation of cutaneous, muscular and visceral pain?

Answer 2

skin = well localised, pricking/stabbing

muscle = poorly localised, aching, tender, cramp

viscera = poorly localised (referred to a somatic structure), dull, vague, associated with nausea

Question 3

what potential stimuli can activate nociceptors?

Answer 3

thermal
mechanical
chemical

Question 4

nociceptors are 1st order neurones - true or false?

Answer 4

true - relay info to second order neurones in CNS

Question 5

what type of nerve fibres are nociceptors?

Answer 5

Aδ and C fibres

Question 6

explain the difference in pain response from Aδ and C fibres?

Answer 6

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

Question 7

describe the difference in sensation between first “fast” pain from Aδ fibres and slow pain from C fibres?

Answer 7

first pain = stabbing, pricking sensation

second pain = burning, throbbing, cramping, aching sensations

Question 8

what receptors can pick up noxious thermal stimuli?

Answer 8

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

Question 9

what receptors do noxious chemical stimuli activate?

Answer 9

H+ = acid sensing ion channels (ASICs)
ATP = P2X and P2Y receptors
bradykinin = B2 receptors

Question 10

what temperatures activate Aδ type I fibres?

Answer 10

Aδ type I = 53 degrees

Aδ type II or C = 43

Question 11

what do efferent signals to nociceptor nerve endings cause?

Answer 11

release of pro-inflammatory mediators - calcitonin gene related peptide (CGRP) and substance P

these mediators contribute to neurogenic inflammation

Question 12

what can noxious stimulation cause in the long term?

Answer 12

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)

Question 13

explain the synaptic connection between the 1st and 2nd order neurone in nociception?

Answer 13

AP opens voltage-gated Ca2+ channels
Ca2+ influx 
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 
new AP

Question 14

where in the dorsal horn of the spinal cord do Aδ and C fibres terminate?

Answer 14

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

Question 15

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?

Answer 15

Aβ - proprioceptive

Question 16

where does visceral pain come from?

Answer 16

coverings of organs eg pleura / peritoneum

when these are stretched / twisted / ischaemic = pain

no pain if cut / burnt

Question 17

what nerve pathways are followed by visceral afferents from nociceptors before entering the dorsal horn of spinal cord?

Answer 17

follows sympathetic pathways

Question 18

what is viscerosomatic pain and how does it present?

Answer 18

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)

Question 19

pain evoked by activity in nociceptors (C and Aδ- fibres) can be reduced by activity in Aβ fibres - true or false?

Answer 19

true - this details the gate control theory

patient often finds that focussing in low threshold activity involving Aβ fibres distracts them from pain

Question 20

what is gate control theory?

Answer 20

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

Question 21

how do Aβ fibres cause no projection from the 2nd order neurone?

Answer 21

they excite an inhibitory interneurone, which then inhibits the projection of any signal