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BB2 > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

1
Q

What is pain? What type of information is it usually associated with?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage. A cerebral construct - a perception usually associated with tissue-damaging stimuli.
Nociceptive information

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2
Q

What are the physiological mechanisms of pain?

A

Transduction
Transmission
Perception
Modulation

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3
Q

What is transduction?

A

Noxious stimuli translated into electrical activity at sensory nerve endings.

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4
Q

What is transmission?

A

Propagation of impulses along pain pathways

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5
Q

What is perception?

A

Discrimination/affect

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6
Q

What is modulation?

A

Positive and negative modulation occurs. Transduction, transmission and perception are modified.

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7
Q

What is another name for acute pain?

A

Normal or nociceptive

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8
Q

What is a nociceptor?

A

A sensory neuron transducing potentially harmful stimuli. Normal pain results from activity of these.

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9
Q

What are the two main nociceptors involved?

A

C fibres

A delta fibres

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10
Q

What do the membranes of nociceptors contain that allow response to noxious stimuli?

A

Receptor proteins

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11
Q

What are the following receptor proteins for?
TRPV1
TRPM8
ASIC

A

Hot stimuli
Acid
Cold stimuli

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12
Q

Diabetes causes peripheral neuropathy. What does this result in the lack of?

A

Pain fibres

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13
Q

What are the A delta fibres for?

A

Sharp pricking fast pain (thermal and mechanical)
Precise localisation of stimulus
Reflex withdrawal

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14
Q

What are the two broad classes of C fibres?

A

Peptidergic

Peptide-poor

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15
Q

What are C fibres for in general?

A

Slow burning pain

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16
Q

What do peptidergic C fibres release peripherally? What does this promote?

A

Peptides e.g. substance P and CGRP

Inflammatory responses and healing

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17
Q

What is special about peptide-poor C fibres?

A

They have distinct receptors and projections e.g. P2X3 ATP receptors

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18
Q

What type of nociception for peptidergic fibres? What type for peptide-poor fibres?

A

Thermal

Mechanical

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19
Q

What are the main two lamina that A delta and C nociceptors connect to?
Which horn is this?

A

I and II

Dorsal horn

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20
Q

What is NaV1.7?

What does loss of it cause?

A

A sodium channel sub-unit

Congenital indifference to pain

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21
Q

What does loss of mutation of NGF receptor trkA cause?

A

Congenital insensitivity to pain with anhydrosis (CIPA) due to loss of C fibres.

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22
Q

Where does the lateral spinothalamic tract end? (3) What for? Where does it not end?

A

Limbic system - subjective sensations of pain and pleasure
Reticular formation - pain-induced arousal and descending control of nociceptor input
Intralaminar (reticular) nuclei of thalamus - alerting cerebral cortex and focus of attention on pain

NOT the VPL (ventral posterolateral nucleus of the thalamus)

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23
Q

The unpleasant character of pain is mediated via projections to what system?

A

Limbic

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24
Q

What lamina do C fibres innervate? (3)

A

I and inter-neurons in lamina II (they also innervate lamina V through these inter-neurons)

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25
Q

What lamina do A delta fibres innervate?

A

Lamina I and V projection neurons

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26
Q

From where do projection neurons in lamina V receive input?

A

A beta fibres (touch) - direct input
C fibres - indirect input via inter-neurons
A delta fibres

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27
Q

Where do axons of projection neurons decussate close to? Where do the axons travel after decussating?

A

Where the nociceptors enter the spinal cord

In the anterior spinothalamic tract (lamina V) and lateral spinothalamic tract (lamina I)

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28
Q

What do projection neurons carry and to where?

A

Pain message onward from the primary afferent

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29
Q

What is the anterior spinothalamic tract also known as?

A

‘Neo’spinothalamic tract

30
Q

What does the anterior spinothalamic tract subserve?

A

First, discriminative aspects of pain – e.g. move arm!

31
Q

Anterior spinothalamic tract - where is the main projection to? What nuclei does it come from? What type of information does this give about the noxious stimulus?

A

Primary somatosensory cortex
Ventral posterior lateral (VPL) nucleus and ventral posterior medial (VPM) nucleus
Localisation & physical intensity

32
Q

What other two projections are there from the anterior spinothalamic tract? Where do they provide input to?

A

Ventral posterior inferior (VPI) nucleus - input to secondary somatosensory cortex

Central lateral (CL) nucleus (reticular and limbic associated areas) - input to sites for cognitive function (prefrontal cortex and striatum) AND sites for emotion (anterior cingulate cortex)

33
Q

What is the lateral spinothalamic tract also known as?

A

‘Paleo’ spinothalamic tract

34
Q

What does the lateral spinothalamic tract subserve?

A

Second, punishing aspects of pain e.g. ouch, that hurts!

35
Q

What fibres innervate projection neurons in lamina I?

A

C fibres

A delta fibres

36
Q

Lateral spinothalamic tract - what nuclei are involved? (3)

Where do they project to?

A

Mediodorsal nucleus –> anterior cingulate cortex
Posterior nucleus –> anterior/rostral insula
Ventral medial nucleus –> anterior/rostral insula

37
Q

What collateral projections does the lateral spinothalamic tract have? (4)

A

Spinal circuitry (for reflexes)
Reticular formation
Periaqueductal gray
Parabrachial nucleus

38
Q

What does the lateral spinothalamic tract project to the reticular formation for?

A

Arousal and alerting cortex

39
Q

What does the lateral spinothalamic tract project to the periaqueductal gray for?

A

Descending pain modulation

40
Q

Where is the parabrachial nucleus?

Where does it project to?

A

Pons

Amygdala

41
Q

What is the role of the amygdala? (2)

A 
Limbic activation (memory)
Autonomic integration and response (w/ insular cortex)
42
Q

What is the role of the insula? (3)

A

Interoception (detects internal regulation responses e.g. hunger)
Homeostatic adjustment
Emotion

43
Q

What are the four cardinal signs of inflammation?

A

Calor
Rubor
Dolor
Tumor

44
Q

What does normal acute pain result from?

A

Nociceptor activity

45
Q

Define acute pain.

A

Acute pain is of sudden onset, usually the result of a clearly defined cause. It resolves with the healing of its underlying cause. It enables protection and facilitates healing.

46
Q

What is fast pain?

What is slow pain?

A

Fast - sharp pain conveyed by A delta fibres, elicits a reflexive withdrawal
Slow - burning, lingering, emotionally charged pain

47
Q

What is peripheral sensitisation?

A

Increased sensitivity to afferent nerve stimuli. It can occur as a result of inflammation. It can cause hyperalgesia, allodynia and spontaneous pain.

48
Q

Define hyperalgesia.

A

Abnormally heightened sensitivity to pain

49
Q

Define allodynia.

A

Pain following non-noxious stimuli

50
Q

In peripheral sensitisation, due to effects of inflammatory mediators, nociceptors show reduction in ____ and increase in _____. Some nociceptors become tonically _____.

A

Activation threshold
Responsiveness
Active

51
Q

Prostaglandins play an key role in what type of pain?

A

Inflammatory

52
Q

What enzymes do NSAIDs target?

A

COX-1 and COX-2

53
Q

What do COX-1 and 2 use as a substrate for prostaglandin synthesis?
What releases this substrate? What type of drugs target this?

A

Arachidonic acid
Phospholipase A2
Steroids

54
Q

COX-1 is present in tissue at ___ levels

COX-2 is induced during _____

A

Low

Inflammation

55
Q

How do prostaglanadins sensitise C fibres? (2)

A

Increasing numbers of other receptors

Increasing the number of open sodium channels

56
Q

Prolonged nociceptor input produces an increase in excitability of…
This causes modified responsiveness.

A

Dorsal horn projection

57
Q

Describe central sensitisation.

A

There are enhanced responses and even low level inputs produce responses.
It causes pain - allodynia, secondary hyperalgesia and spontaneous pain.
It differs from peripheral sensitisation as it extends outside the region of flare.

58
Q

What is flare due to?

A

Release of peptides by C-fibres and other local inflammatory mediators

59
Q

How many weeks does pain have to last for it to be classified as chronic?

A

12 weeks

60
Q

What does maladaptive mean in terms of pain?

A

It continues past the healing phase following an injury

61
Q

Chronic pain is normally associated with an underlying condition/arises from nociceptive pain? - True or False

A

True

62
Q

Maladaptive pain is due to…?

A

Abnormal activity in the neural system

63
Q

Are normal analgesics effect for maladaptive pain?

A

No

64
Q

How is maladaptive pain treated? Does it respond well to treatment?

A

Anticonvulsants
Anti-depressants
No - often resistant to treatment

65
Q

What is neuropathic pain due to?

A

Injury/dysfunction in PNS or CNS

66
Q

What is dysfunctional pain due to?

What is it characterised by?

A

No known lesion or inflammation

Hyperalgesia, allodynia, spontaneous pain

67
Q

Where does pain modulation occur? (4)

A

Cortex
From the brain/brainstem
Spinal cord (central sensitisation)
Periphery (inflammation)

68
Q

Where does endogenous modulation occur?

A

At the spinal cord level

69
Q

Superior parietal cortex – insula – amygdala path is for…?

A

Cognitive/attention control/intensity of pain

70
Q

Anterior cingulate cortex – pre-frontal cortex – periaqueductal gray path is for…?
What drug is it sensitive to?

A

Emotion/unpleasantness

Naloxone

71
Q

What fibres does acupuncture activate?

What pathway does it work through?

A

Aδ fibres

Periaqueductal gray mediated control

72
Q

What is the basis of the TENS (transcutaneous electrical nerve stimulation) machine?

A

Stimulation of non-noxious afferents (or mildly noxious afferents) - these stimulate lamina II inter-neurons.

BB2 (32 decks)

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