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Flashcards in Pain Deck (32):
1

What is pain?

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

2

What is the difference between nociception and pain?

Nociception is a sensory process

Pain is a higher order process that requires higher order processing

3

Describe the process of nociception?

1. Transduction: nociceptors detect physical force on tissues

2. Transmission: peripheral and central, in lateral spinothalamic tract

3. Perception: sesnory and emotional, cortical input

4. Modulation: can interfere with transmission of information or act at a higher level

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4

What are the two classes of adaptive/protective pain?

Nociceptive pain

Inflammatory pain

5

What are the two classes of maladaptive/pathological pain?

Neuropathic pain

Functional pain syndromes

6

Briefly describe the broad pathway for nociceptive pain?

Noxious stimulus (temperature, force, chemical) > nociceptor sensory neuron > spinal cord > response (withdrawal reflex) > pain (adaptive, high-threshold)

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7

Describe the somatosensory neurons involved in nociception?

Unmyelinated C-fibres: thin, slow transmission, enter at most supericial layers of dorsal horn

Myelinated Ad fibres: thin, fast transmission, enter at superficial and deeper layers of dorsal horn

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8

Why are two different fibre tyes involved in nociception?

Ad fibres are rapid, and give info about sharp pain

C fibres are slower, and give info about slow, burning pain

First and second pain

 

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9

How do second order neurons project to the brain in the nociceptive pathway?

Anterolateral tract 

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10

Why do spinal nociceptive reflexes not result in pain?

Nociceptive fibres only make connections in the spinal cord 

They connect to motor neurons to cause muscle contractions 

Brain not involved > no pain 

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11

Describe the relationship between pain, time and stimulus intensity for nociceptive pain?

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12

What is required for the perception of pain?

Sensory info must be decoded in the cortex

13

Briefly describe the broad pathway of inflammatory pain?

Peripheral inflammation > inflammaory cells and tissue damage stimulate nerve endings > spinal cord > spontaneous pain, pain hypersensitivity > adaptive, low-threshold pain

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14

What is the stimulus for inflammatory pain?

Inflamed or damaged tissues release nociceptor sensitisers

'infalmmatory soup'

15

Which types of receptors are involved in nociceptor transduction?

Ion channels 

GPCRs

 

16

What is sensitisation?

Two types: peripheral and central

Peripheral sensitisation involves acting on nerve endings to make them more sensitive to stimuli

Central sensitisation involves acting on on the central pain system to make it more sensitive

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17

What are the outcomes of central and peripheral sensitisation?

Peripheral sensitisation: from innocuous stimulus > primary allodynia; from noxious stimulus > primary hyperalgesia

Central sensitisation: from innocuous stimulus > secondary allodynia; from noxious stimulus > secondary hyperalgesia

 

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18

What are hyperalgesia and allodynia?

Hyperalgesia: an increased response to a normal stimulus

Allodynia: a painful response to a normally innocuous stimulus 

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19

What is secondary hyperalgesia?

Following central sensitisation in the spinal cord, the hyperalgesia may spread to areas which are not physically damaged

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20

Describe the relationship between pain, time and stimulus intensity for inflammatory pain?

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21

Which class of pain are peripheral and central sensitisation associated with?

Inflammatory pain

22

Describe the broad pathways of neuropathic and dysfunctional pain?

Neuropathic pain: neural lesion > spontaneous pain and hypersensitivity > maladaptive, low-threshold pain, disease state

Dysfunctional pain: no neural lesion > spontaneous pain and hypersensitivity > maladaptive, low threshold pain, disease state 

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23

Describe how/why peripheral neuropathic pain occurs?

Damage to sensory nerves > changes in terminal fields > start to generate pain signals without sensory stimulation

Can happen anywhere in pathway 

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24

Describe the relationship between pain, time and stimulus intensity for neuropathic pain?

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25

Using fMRI imaging, which parts of the brain appear to be activated when someone is in pain?

Sensorimotor part of cortex

Emotional areas

Info coming up through spinal cord separates in thalamus and splits into these two areas

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26

Give examples of the major classes of centrally acting analgesic drugs?

Opioids

NSAIDs

Anticonvulsants

Cannabinoids

27

How do analgesic drugs work?

Some interfere with transmission of sensory information from sensory neurons to projection neurons, therefore blocking pain related information transmission 

 

Some activate the PAG pathway, which relays through the medulla then projects to the dorsal horn 

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28

Describe endogenous pain modulation?

System is bimodal - can facilitate pain as well as inhibit pain

 

29

Describe the relationship between anxiety/fear and apin?

Anxiety and fear can induce hypoalgesia 

Endogenous inhibition of pain sensitivity 

30

Describe the top-down psychological modulation of pain?

Cortical areas (anterior cingulate, PFC and insula) can alter pain sensitivity 

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31

Describe the effects of placebo and nocebo on pain?

Substituting a placebo for an active treatment alters pain matrix activity in neuroimaging and produces genuine analgesia via endogenous pain modulation (reduced or prevented by opioid antagonists)

Expectations of pain produce activity changes, but these correlate with nocebo hyperalgesia

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