302 Physiology of pain

Question 1

What are different types of pain?

Answer 1

1. Nociceptive (somatic or visceral)
2. Inflammatory
3. Neuropathic

Question 2

What is nociceptive pain?

Answer 2

A physiological response to real or threatened non-neural tissue damage
-Threat is thermal, chemical, or mechanical
-Reversible pain once the insult is removed

Question 3

Which fibres are stimulated in nociceptive pain?

Answer 3

C fibres and Aδ fibres on peripheral nerves

Question 4

What is somatic nociception?

Answer 4

Activation of nociceptors in skin, muscles, bones, joints, and connective tissues

Transmitted along A-delta and C fibres

Somatic pain – sharp or dull pain. Exacerbated by movement.

Question 5

What is visceral nociception?

Answer 5

-Activation of nociceptors in internal organs
-Transmitted along autonomic fibres

Visceral pain – poorly localised, deep, squeezing, cramping pain, dull, sickening.

Associated autonomic symptoms – nausea, vomiting, sweating

Question 6

What is inflammatory pain?

Answer 6

-Response of the somatosensory nervous system to tissue damage and inflammation.

In the periphery, increased inflammatory mediators (cytokines and chemokines) sensitize local nociceptors:
Lowers threshold for responsiveness (peripheral sensitization).
Results in activation of pathways after innocuous input and in exaggerated responses to noxious stimulation.

The plasticity that underpins these changes is rapid (occurring in minutes).
Inevitable consequence of surgery and tissue trauma.

Upregulation of nociception normally resolves as wound healing occurs.

Question 7

What is neuropathic pain?

Answer 7

A lesion or disease of the somatosensory nervous system.

Impacts on function and causes structure changes in the somatosensory nervous system.

The result is a combination of sensory loss and increased responsiveness to both noxious and innocuous stimuli.

Question 8

What is allodynia?

Answer 8

Pain after non-painful stimuli

Question 9

What is hyperalgesia?

Answer 9

Heightened pain after painful stimuli

Question 10

What is hyperpathia?

Answer 10

An eruptive pain extending beyond the duration of a stimulus

Question 11

What does neuropathic pain feel like?

Answer 11

Electric shock
Burning
Cramping
Constant
Fleeting
Provoked

Question 12

Name some nociceptors

Answer 12

Free nerve ending
Merkel disk
Meissner’s corpuscle
Pacinian corpuscle
Hair follicle receptor

Question 13

What does a Merkel disk detect?

Answer 13

Gentle touch

Question 14

What do Meissner’s corpuscles detect?

Answer 14

Vibrations
Most sensitive to low frequency vibrations

Question 15

What do Pacinian corpuscles detect?

Answer 15

Vibrations transmitted to the skeleton

Question 16

What does a free nerve ending detect?

Answer 16

Temperature, mechanical stimuli (touch, pressure, stretch) or danger (nociception)

Question 17

What is the difference between nociception and pain?

Answer 17

Nociception: how signals about possible tissue damage get from the site of injury to the brain.

Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such.

Question 18

What factors feed in to create pain from nociception?

Answer 18

Beliefs
Psychological factors
Cultural issues
Other illnesses
Personality
Social factors

Question 19

Describe the nociceptive pathway

Answer 19

4 steps:
Periphery
Spinal cord
Brain
Modulation

Question 20

What happens physiologically in tissue injury?

Answer 20

-Release of chemicals soup
-Stimulates nociceptors.
-Sensitizes nociceptors.
-Signal travels in Aδ or C nerve to spinal cord

Question 21

What does ‘group A-C’ nerve fibre classification refer to?

Answer 21

(The level of myelination)

Group A – heavily myelinated. Carry quick, sharp pain

Group B – moderately myelinated
Usually general visceral afferent fibres and preganglionic nerve fibres of the autonomic nervous system

Group C – unmyelinated. Carry slow, achy pain

Question 22

What is the effect of myelin on nerves?

Answer 22

Myelination allows the formation of nodes of ranvier that speeds up the activity along the axon via saltatory conduction

Question 23

What happens when the pain signal reaches the spinal cord?

Answer 23

1. Dorsal horn is the first relay station.
2. Aδ or C nerve synapses with second order neurone.
3. Second order neurone travels up opposite side of spinal cord

Question 24

What is the tract of lissauer for?

Answer 24

Afferent fibres reach the spinal cord and use it to ascend or descend

Question 25

Where does the spinothalamic tract terminate?

Answer 25

At the thalamus

Question 26

Where does each of the pain fibres synapse?

Answer 26

The grey matter of the dorsal horn that is divided into rexed laminae

A-delta fibres
terminate in Lamina 1 and 5.
Synapse directly with the 2nd order neurones that make up the ascending tracts.

C-fibres
predominantly synapse with neurones in Lamina 2 (substantia gelatinosa).
often synapse indirectly via interneurones (which can be wide dynamic range neurones)

Question 27

How do pain signals get up the spinal cord?

Answer 27

After crossing to the contralateral cord (decussation), 2nd order neurones ascend the spinal cord in several tracts.

Most important are spinothalamic tract and the spinoreticular tract

Question 28

Describe the divisions of the spinothalamic tract

Answer 28

Lateral - Neo (new)-spinothalamic tract.
It’s the discriminative aspect of pain perception.

Medial - paleo (primitive)-spinothalamic tract
It’s the autonomic and unpleasant emotional component of the pain experience

Question 29

Where is the ventral posterior lateral (VPL) nucleus found ?

Answer 29

In the thalamus

Question 30

Where does the lateral spinothalamic tract terminate?

Answer 30

VPL nucleus in the thalamus

Question 31

Where does the medial spinothalamic tract terminate?

Answer 31

It’s a polysynaptic pathway that sends projections to PAG (periaqueductal grey) matter, hypothalamus and reticular system in the midbrain before reaching the medial thalamus

Question 32

Where does the spinoreticular tract terminate?

Answer 32

In reticular formation of medulla and pons and then from there to the thalamus

Project diffusely to entire cerebral cortex. Pain reaches conscious level and promotes behavioural arousal.

Question 33

What happens when the nociception reaches the brain?

Answer 33

It becomes pain

The thalamus sends signals to:
Sensory cortex
Limbic system
Brainstem

Question 34

How does the brain create a perception of pain?

Answer 34

3rd-order neurones project from thalamus to somatosensory cortex.

Primary somatosensory projection (S1) - mediate localisation of the pain stimulus

Secondary somatosensory projection S2 - ?stimulus intensity

Question 35

What is the role of the limbic system in pain?

Answer 35

Involved in creation of emotion, behaviour, and memory.

Insula
major hub for visceral nociceptive inputs
assessment of nociceptive stimulus intensity

Anterior Cingulate Cortex (ACC)
the frontal part of the cingulate cortex that resembles a “collar” surrounding the frontal part of the corpus callosum)
Functions: attention and response

ACC has connections to deep ancient structures:
Amygdala
Hippocampus
Hypothalamus

Question 36

How are nociceptive signals modulated?

Answer 36

-Melzack and Wall’s gate control theory
-Descending inhibitory pathways

Question 37

How does the Melzack and Wall’s gate control theory of pain work?

Answer 37

Non-painful input closes the “gates” to nociceptive input prevents AP traveling to the CNS

Question 38

What happens in descending inhibitory pathways?

Answer 38

Originate from supra-spinal structures:
periaqueductal gray
reticular formation
nucleus raphe magnus

Endogenous opioid receptors heavy expressed here.
Serotonin and NA are key neurotransmitters in this pathway.

Inhibit transmission of nociception at level of DH.

Question 39

How can anti-depressants modify the nociceptive pathway?

Answer 39

Because serotonin and NA are key transmitters here – TCAs and SNRIs increase the levels of these transmitters and ‘turn up’ your descending inhibitory action