Lecture 6- Nociception and pain 1

Question 1

Transduction

Answer 1

• Process of creating an electrical signal from a physical stimulus
• Activation of receptors allows ions to pass across nerve cell membrane
• Ion channel response&raquo_space; influx + ions&raquo_space; electrical charge across membrane&raquo_space; if > threshold&raquo_space; action potential

Question 2

Afferent nerves

Answer 2

•	A-beta:
o	Light touch and vibration
o	Fast conducting (myelinated)
o	Low stim threshold
•	A-delta and C:
o	Noxious stim
o	Slower (thinly or unmyelinated)
o	High stim threshold

Question 3

Somatosensory pathways

Answer 3

• Dorsal column of SC = discrim touch and proprioception

* Anterolateral = discrim info pain, temp and course touch

Question 4

Nociceptors (1st order neurons)

Answer 4

•	A-delta
o	Thinly myelinated
o	Polymodal- Thermal, mechanical and chemical
o	First or fast pain- sharp or pricking
•	C
o	Unmyelinated
o	Polymodal
o	Prolonged burning or dull pain- second or slow
•	Silent nociceptors
o	Active when tissue damaged or inflamed

Question 5

Spinothalamic pathway

Answer 5

• Fast pain- sharp, localising
• Lateral system
• Conscious relay to sensory cortex
• Primary neurotrans = glutamate
• A-delta synapse dorsal horn

Question 6

Spinolimbic/ spinoreticular/ spinomesencephelic pathways

Answer 6

• Slow pain- dull, throbbing, poorly localised
• Medial system
• Transmit info extent of injury and bodies response
• Primary neurotrans = substance P
• C synapse interneurons in dorsal horn

Question 7

Medial pain system

Answer 7

• Spinomesencephalic- head turning to noxious source, activates descending tracts that modulate pain (automatic movements and withdrawal)
• Spinoreticular- arousal, attention, sleep/awake cycles
• Spinolimbic- affective dimensions of pain
• Integration of noci + homeostatic and autonomic processes

Question 8

Peripheral sensation

Answer 8

1. A-delta or C activation
2. Presence of inflammatory mediators
3. Sensitisation of peripheral nociceptors- more overall nociception activation
4. Recruitment of dormant multimodal nociceptors- due to exposure to inflam soup
5. Repeated nociceptive stimulation- release of substance P and CGRP, further stims inflam process

Question 9

Hyperalgesia

Answer 9

• experiencing more pain than stimulus should generate
• peripheral sensation = primary
• central = secondary

Question 10

Central sensitisation

Answer 10

• enlargement of receptive fields
• increase responses to >threshold stim (hyperalgesia)
• possible development of spontaneous activity (neurogenic pain)
• reduction threshold for activation from periph stim (hyperal)
• enhanced function of noci pathway neurons

Question 11

Wind-up

Answer 11

• barrage nociceptive input onto 2nd order neuron in DH leads to prolonged discharge
• can’t repol before next stim
• progressive increase in number of action potentials evoked by stim
• activation of NMDA receptor
• repetitive wind-up = long-term increase in synaptic transmission efficacy = long-term potentiation

Question 12

Allodynia due to central sensitisation issues

Answer 12

• physical changes occur in DH:
o death inhib neurons
o sprouting of A-beta terminals where normally only A-delta or C are
o conversion wide dynamic range neurons- respond to noxious and innocuous stim
o novel synapses between A-beta and central noci neurons
• result:
o additional/amplified noci info = secondary hyperalgesia
o innocuous aff may stim noci = allodynia