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MBChB - Y2 - Systems - Nervous System > Physiology and Pathophysiology of Pain > Flashcards

Physiology and Pathophysiology of Pain Flashcards

1
Q

What is pain?

A

Pain is an unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage or both

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2
Q

What is noiciception?

A

The detection of tissue damage by specialized transducers connected to A - delta and C fibers

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3
Q

What part of the noiciceptor detects pain?

A

Free nerve endings

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4
Q

What type of stimuli do noiciceptors respond to?

A

Thermal

Chemical

Mechanical

Noxious stimuli

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5
Q

Which type of nerve fibre is responsible for fast pain? Slow pain?

A

Fast pain - A delta

Slow pain - C fibres

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6
Q

What are the three types of neurone found predominantly in the grey matter?

A

Low threshold mechanoreceptive neurons (layer 3 and 4) - receive input from A beta fibres

Noiciceptive specific neurons (layer 1 and 2) receiving input from C and A delta fibres

WDR (wide dynamic range) (layer 5) - main input is A beta responds to both noxious and non-noxious stimuli via interneurons.

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7
Q

Where do primary noiciceptive afferent impulses primarily end?

A

In the dorsal horn

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8
Q

What is the anterior spinothalamic tract responsible for?

A

Sensation of simple touch

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9
Q

What is the lateral spinothalamic tract responsible for?

A

Conveys fast and slow pain

(pain and temperature sensation)

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10
Q

Which rexed lamina does the spinothalamic tract arise in?

A

Arises in the rexed lamina 1,2 and 5

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11
Q

Where does the lateral spinothalamic tract end?

A

Terminates in the ventroposterior thalamic nuclei

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12
Q

Where does the ventroposterior thalamic nuclei feed into?

A

The somatosensory cortex to facillitate the spatial, temporal and intensity discrimination of painful stimuli

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13
Q

Where does the ventral spinothalamic tract project?

A

To the medial thalamic nuclei

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14
Q

Where does the medial thalamic nuclei project to?

A

Cortical regions such as anterior cingulate and insular cortex as well as other parts of the limbic system

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15
Q

Summary

A
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16
Q

Where does pain perception occur?

A

In the somatosensory cortex

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17
Q

Where do descending pathways arise from that usually descrease the pain signal?

A

Arise from the periaqeductal grey matter

travel from the brain to the dorsal horn

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18
Q

What is hyperalgesia?

A

Increased perception of pain or even perception of non-noxious stimuli as noxious stimuli

19
Q

When does hyperalgesia happen?

A

Happens when there is a tissue injury and inflammation

20
Q

What do the terms primary hyperalgesia and secondary hyperalgesia mean?

A

Primary - hyperalgesia at the site of injury

Secondary - hyperalgesia in surrounding uninjured tissue

21
Q

Define allodynia

A

Central pain sensitization following normally non-painful stimulation

Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.

22
Q

What is the difference between allodynia and hyperalgesia?

A

Allodynia - decreased threshold for response

Hyperalgesia - Exaggerated response to stimuli

23
Q

How does spontaneous pain compare to allodynia and hyperalgesia?

A

Spontaneous pain doen’t affect the sensation of pain - it results in spontaneous activity in nerve fibres

24
Q

What is the main difference between peripheral sensitization and central sensitization?

A

Central sensitization happens at the level of the spinal cord

Peripheral sensitization causes sensitivity to heat

25
Q

What are the three components of central censitization?

A

Wind-up

Classical

Long-term potentiation

26
Q

What happens during Wind up?

A

C fibres are influenced by substance P (their threshold is lowered)

C fibres are now more sensitive and are more likely to depolarize

There is also an increase in the receptive field of C fibres

27
Q

Which neurones are involved in wind up?

A

Only the neurones taking part in the synapses with primary afferent input

28
Q

When does wind up manifest and when does it terminate?

A

Manifests over the course of a stimulus and terminates with that stimulus

29
Q

How does the classical - central sensitisation mechanism work?

A

Involves opening up of new synapses as a result of a strong enough stimuli to elicit the response.

If the intensity is strong enough then it occurs immediately with the stimuli and can outlast the duration of the stimuli

Results in secondary hyperalgesia

Once activated, it can be maintained even by low intensity of the offending stimuli

30
Q

What neurotransmitters and receptors are associated with classical sensitization?

A

NMDA receptor activation by glutamate is known to trigger a series of changes resulting in classical central sensitization

31
Q

Which synapses are involved in long-term potentiation?

A

Involves mainly the activated synapses

32
Q

What type of stimuli does long - term potentiation result from?

A

Results from very intense stimuli

33
Q

What are the receptors and transmitters for long-term potentiation?

A

The mechanism is involves both AMPA and NMDA receptor activation by glutamate.

34
Q

What is the result of suprasegmental central sensitization of pain?

A
35
Q

What is the difference between chronic pain and acute pain?

A

In chronic cases the presence of noxious stimuli is not essential and the source can be nociceptive, neuropathic or mixed

36
Q

What is nociceptive pain?

A

A sensory experience that occurs when specific peripheral sensory neurones (nociceptors) respond to noxious stimuli

37
Q

When does nociceptive pain normally end?

A

Usually resolves when damaged tissue heals

38
Q

What is neuropathic pain?

A

Pain initiated or caused by a primary lesion or dysfunction in the somato-sensory nervous system

39
Q

Where does neuropathic pain occur?

A

•The painful region may not necessarily be the same as the site of injury – pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain)

40
Q

Is neuropathic pain more likely ot be acute or chronic?

A

Chronic

Ulinke nociceptive pain it responds poorly to conventional analgesics

41
Q

How can we reduce transduction of pain?

A

NSAIDS

Ice

Rest

LA blocks

42
Q

How do we reduce transmission of nociception?

A

Nerve blocks

Drugs

  1. Opioids
  2. Anticonvulsants

Surgery

  1. DREZ - dorsal root entry zone (The surgery destroys the area where damaged nerves join the central nervous system, thereby interfering with inappropriate pain messages from nerves to the brain.)
  2. Cordotomy - cutting nerves of spinal cord
43
Q

How do we alter the perception of pain?

A

Education

Cognitive behavioural therapy

Distraction

Relaxation

Graded motor imagery

Mirror box therapy

44
Q

How can we manipulate descending modulation?

A

Placebos

Drugs

  • Opioids
  • Antidepressants

Surgery

  • Spinal cord stimulation

MBChB - Y2 - Systems - Nervous System (48 decks)

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