13 - Pain

Question 1

Example of a definition of pain

Answer 1

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

Question 2

Different types of pain 1 2 3

Answer 2

1) Nociceptive pain 2) Inflammatory pain 3) Neuropathic pain

Question 3

Chronic pain

Answer 3

Pain for three of the past six months. A large proportion of people with chronic pain don’t respond to treatment.

Question 4

Relationship between pain and nociception.

Answer 4

Not synonymous. Nociception is nerve detection of noxious stimulus. Pain is cortical recognition thereof.

Question 5

Stages of nociception 1 2 3 4

Answer 5

1) Transduction (receptor detection of H+. heat. noxious cold, pressure, chemicals, etc) 2) Transmission (peripheral and central) 3) Perception (sensory/discriminative, emotional) 4) Modulation

Question 6

Sensory/discriminative pain

Answer 6

How intense pain is, where it is. Carried through lateral spinothalamic tract to the lateral thalamus.

Question 7

Spinal tract through which nociceptive information travels to brain

Answer 7

Spino-parabrachial tract, lateral spinothalamic tract. Travel to the lateral thalamus, limbic centres.

Question 8

Emotional/aversive pain

Answer 8

Emotional perception of pain. Travels through spinoparabrachial tract to limbic centres.

Question 9

Responses to nociceptive pain 1 2 3

Answer 9

1) Pain 2) Autonomic reflexes 3) Withdrawal reflex

Question 10

Nociceptor nerve endings

Answer 10

C-fibres, A-delta fibres.

Question 11

Location of nociceptive neuron cell bodies

Answer 11

In dorsal root ganglia, trigeminal ganglia (for pain of head and face)

Question 12

C-fibre morphology

Answer 12

Unmyelinated. Thin (under 1.5 micromete) Slow transmission (under 3m/s)

Question 13

A-delta fibre morphology

Answer 13

Myelinated. Thin (1.5 - 4 micrometes) Medium-fast transmission (3-30m/s)

Question 14

Temperature around which a heat nociceptor will start being stimulated

Answer 14

~42 degrees. High-threshold.

Question 15

Difference in type of pain from C-fibres and A-delta fibres

Answer 15

C-fibres give slow, burning pain. A-delta give sharp pain.

Question 16

*First and second pain

Answer 16

FIRSTSECONDPAIN

Question 17

*Projection of second-order neurons to brain via anterolateral tract

Answer 17

Nociceptor afferents synapse ipsilaterally with a spinal interneuron, which crosses contralaterally and ascends to brain in anterolateral system.

Question 18

Inflammatory pain

Answer 18

Similar to nociceptive pain, but system is modulated by inflammatory mediators released by immune cells (hyperalgesia). System evolved to protect damaged tissues (eg: with behaviour).

Question 19

‘Inflammatory soup’

Answer 19

Inflamed or damaged tissues release nociceptor sensitisers.

Question 20

*TRP channel

Answer 20

Transient receptor potential channel. TRPV1 is a nociceptive transducer.

Question 21

Stimuli that TRPV1 often responds to

Answer 21

Noxious heat, acid, reactive chemicals.

Question 22

TRP channel responsible for detecting environmental cold

Answer 22

TRVM8 (EG activated by menthol)

Question 23

What causes secondary allodynia to come about?

Answer 23

Central sensitisation by inflammation. An innocuous stimulus of a low-threshold neuron leads to stimulation of sensitised central pathway, leading to secondary allodynia.

Question 24

Difference between hyperalgesia and allodynia

Answer 24

Hyperalgesia is an increased response to a normally painful stimulus. Allodynia is a painful response to a normally innocuous stimulus.

Question 25

Secondary hyperalgesia

Answer 25

Expansion of an area that feels painful from area of initial injury. Sensitisation of adjacent spinal segments, leading to hyperalgesia of area surrounding initial injury.

Question 26

Types of maladaptive pain 1 2

Answer 26

1) Neuropathic pain (neural lesion, positive and negative symptoms. 2) Dysfunctional pain (no neural lesion, no inflammation, positive symptoms). EG migraine (no identifiable pathology apart form the pain itself)

Question 27

*Ways in which peripheral neuropathic pain can airse

Answer 27

Question 28

Parts of the brain involved in pain

Answer 28

Somatosensory cortex, insular cortex, cingulate cortex, amygdala, parabrachial nucleus.

Question 29

*Brain pathways of pain

Answer 29

Question 30

Parts of brain that can modulate pain

Answer 30

Periaqueductal grey matter, rostral ventral medulla

Question 31

Drugs that can act on the periaqueductal grey matter for analgesia

Answer 31

Opioids, NSAIDS (mimic molecules in descending pain pathway)

Question 32

Descending pain pathway

Answer 32

From amygdala, engages in descending pain modulation. Can be modulated by inflammation, analgesic drugs.

Question 33

Effects of anxiety and fear on pain perception

Answer 33

Hypoalgesia.

Question 34

Human cortical areas involved in top-down psychological modulation of pain 1 2 3

Answer 34

1) Anterior cingulate cortex 2) Prefrontal cortex 3) Insula cortex These interact with the periaqueductal grey matter to modulate descending pain pathway

Question 35

Can placebo effect be pharmaceutically reversed?

Answer 35

Yes. Can reverse/prevent with opioid antagonists (EG loxone).

Question 36

Endogenous molecules involved in pain inhibition

Answer 36

Encephalins.

Question 37

Nocebo

Answer 37

Anticipation of pain can lead to hyperalgesia.