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BRAIN AND BEHAVIOUR 2 > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

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The Brain flashcards
1
Q

Define ‘pain’

A

An unpleasant sensory and emotional experience associated with actual, or potential, tissue damage

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2
Q

What is a ‘nociceptor’?

A

A sensory neurone that transduces potentially harmful (noxious) stimuli

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3
Q

What are the four stages in the pain mechanism?

A

Transduction, transmission, perception, modulation

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4
Q

Briefly describe what is meant by transduction in the pain mechanism?

A

This is where the input of potentially harmful stimuli (noxious) is translated into electrical activity at the sensory nerve endings

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5
Q

Briefly describe what is meant by transmission in the pain mechanism?

A

This is where the generated impulse is propagated as impulses along the main nervous pathways

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6
Q

Briefly describe what is meant by perception in the pain mechanism?

A

This involves the interpretation of the pain stimulus, which includes discrimination, effect and providing motivation

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7
Q

Briefly describe what is meant by modulation in the pain mechanism?

A

These stages of pain can be modified either positively or negatively

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8
Q

Which two types of nerve fibres act as nociceptors?

A

A-delta and C-fibres

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9
Q

How do C-fibres and A-delta fibres differ?

A

C-fibres aren’t myelinated and so tend to carry slower pains (second pain such as burning).

A-delta fibres are slightly myelinated so tend to carry the ‘first pain’ which is more acute

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10
Q

What receptor protein must be present on nociceptors for hot stimuli?

A

C fibres which have TRPV1 receptors

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11
Q

What receptor proteins must be present on nociceptors for acid stimuli?

A

C fibres with TRPV1 and ASIC receptors

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12
Q

What receptor proteins must be present on nociceptors for cold stimuli?

A

C fibres with the TRPMbeta receptor

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13
Q

What stimuli do A-delta nociceptors detect?

A

Sharp, pricking, fast pain e.g. thermal and mechanical pain –> reflex response

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14
Q

What stimuli do C-fibre nociceptors detect?

A

Slow, burning pain

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15
Q

What are the two different types of C-fibre nociceptor?

A

Peptidergic and peptide-poor C-fibres

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16
Q

What is the function of peptidergic C-fibres?

A

Cause pro-inflammatory and vasoactive responses generally in response to thermal stimuli. There is peripheral release of substance P and CGRP which is responsible for this.

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17
Q

What is the function of peptide-poor C-fibres

A

Distinctly involved in responding to mechanical stimuli due to the presence of specific P2X3 ATP receptors

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18
Q

What two spinal tracts are involved in the transmission of pain (ascending)?

A

Lateral and anterior spinothalamic tracts

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19
Q

Which spinal laminae do C-fibre nociceptors synapse in?

A

Innervate projection neurones in I,and interneurones in II (to project to lamina V)

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20
Q

Which spinal laminae do A-delta nociceptors synapse in?

A

Innervate projection neurones in lamine I and V

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21
Q

From which laminae does the anterior/neo spinothalamic tract originate?

A

Fibres which synapse in lamina V then ravel in the anterior spinothalamic tract

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22
Q

From which laminae does the lateral spinothalamic tract originate?

A

Fibres which synapse in LAMINA I then travel in the lateral spinothalamic tract

23
Q

What is the role of the anterior spinothalamic tract in pain?

A

To provide the first, discriminative aspects of pain by travelling to the primary somatosensory cortex

24
Q

What is the role of the lateral spinothalamic tract in pain?

A

To provide the second, punishing aspects of pain by adding emotion and quality to the pain

25
Q

Where does the anterior spinothalamic tract synapse in the thalamus?

A

The VPL and VPM (somatosensory) nuclei

26
Q

Where does the lateral spinothalamic tract synapse in the thalamus?

A

Mediodorsal nuclei (Ventrocaudal and Mdvc) and the posterior (medial subnucleus, POm) and ventral medial nucleus (posterior and VMpo)

27
Q

Where do the fibres of the anterior spinothalamic travel from the thalamus?

A

From the VPL and VPM to the primary somatosensory cortex

28
Q

Where do the fibres of the lateral spinothalamic travel from the thalamus?

A

From the mediodorsal nucleus to the anterior cingulate cortex (ACC) involved in emotion and motivation.

From the posterior thalamus to the anterior insula involved in emotion and quality of pain

29
Q

What are the collateral projections of the lateral spinothalamic tract?

A

> Spinal reflexes
Reticular formation in the midbrain - alerts the cortex and PAG to affect descending pain modulation
To the parabrachial nucleus in the pons and then to the amygdala

30
Q

What is the role of the anterior cingulate cortex in pain?

A

Emotional reaction and motivation

31
Q

What is the role of the primary somatosensory cortex in pain?

A

Somatosensory discrimination, location and intensity

32
Q

What is the role of the pre-frontal cortex in pain?

A

Evaluation and cognition

33
Q

What is the role of the insula in pain?

A

Forms a pain ‘map’ alongside homeostatic adjustment and emotion

34
Q

What is the role of the amygdala in pain?

A

Aversion, emotional memory and response

35
Q

What systems are involved in the cognition, intensity and attention aspects of pain?

A

Superior parietal cortex = insula and amygdala

36
Q

What systems are involved in the emotion, placebo and unpleasant perception of pain?

A

Anterior cingulate cortex, prefrontal cortex and PAG

37
Q

Where does pain modulation occur?

A

> In the periphery (peripheral sensitisation)
In the spinal cord (central sensitisation)
From the brain and brainstem
In the cortex

38
Q

What is peripheral sensitisation?

A

In the periphery, nociceptors show a reduction in their activation threshold causing an increase in responsiveness; this is due to change in threshold for sodium channels, potassium channels and TRPV1 channels

39
Q

Explain the mechanism of peripheral sensitisation

A

Phospholipase A cleaves arachidonic acid from cell membranes. COX-1/COX-2 use this as a substrate for PG synthesis. The PGs then sensitise the C-fibres by increasing the numbers of receptors and the number of open sodium channels

40
Q

What is central sensitisation?

A

Prolonged nociceptor input increases the excitability of the projection neurones in the dorsal horn so that it’s activity outlasts the inducing stimulus; there is a greater release of glutamate and peptides.

41
Q

What causes central sensitisation?

A

Prolonged nociceptor input into the DORSAL HORN NEURONE

42
Q

What is the consequence of central sensitisation?

A

Allodynia, secondary hyperalgesia and spontaneous pain (as low threshold A-beta inputs produce a response)

43
Q

What is the gate control theory of pain?

A

You can modulate the transmission of pain by using innocuous stimuli to lessen the pain. USING THE LAMINA II INTERNEURONES

44
Q

Define ‘chronic pain’

A

Pain of more than 12 weeks usually associated with an underlying condition

45
Q

What is ‘maladaptive pain’?

A

A form of pain which occurs due to abnormal activity in the neural system

46
Q

What are the two types of maladaptive pain?

A

Neuropathic and dysfunctional

47
Q

What is ‘neuropathic pain’?

A

Pain that occurs due to dysfunction/injury in the peripheral or central nervous system

48
Q

What is ‘dysfunctional pain’?

A

Pain that occurs due to no known lesion or inflammation

49
Q

What are the causes of maladaptive pain?

A

Injury, stroke, chronic alcoholism, diabetes, infection

50
Q

How may maladaptive pain be treated?

A

Anticonvulsants and antidepressants; normal analgesia is ineffective as their is imbalance in the modulatory systems

51
Q

How does acupuncture work to alleviate pain?

A

Pins activate A-delta fibres which stimulates the PAG to mediate diffuse noxious inhibitory control of pain

52
Q

How does TENS work to alleviate pain?

A

Non-noxious inputs act to stimulate the lamina II interneurones to facilitate gate-control theory

53
Q

What are the four signs of inflammation?

A

Heat, redness, pain, swelling

BRAIN AND BEHAVIOUR 2 (31 decks)

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