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MD1 Neuroscience > Pain > Flashcards

Pain Flashcards

1
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual/potential tissue damage

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2
Q

What are some physiological stimuli for nociceptive pain?

A

Mechanical
Termal
Chemical injury

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3
Q

What are some clinically relevant stimuli for nociceptive pain?

A 
Abnormal mechanical forces 
- Osteoarthritis
Organ injury
- Angina
- Ischaemic claudication
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4
Q

What is pain proportional to?

A

Strength of stimulus

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5
Q

Describe the nociceptive pathway in general

A 
Nociceptor encodes info
Relayed to spinal cord/brainstem
Travels via ascending pathways
Much of info goes through thalamus
Up to areas of cortex
Converted into pain perception
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6
Q

Is nociception different to somatosensation?

A

No, it’s a subclass

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7
Q

What is the threshold for nociceptors?

A

High threshold

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8
Q

What do nociceptors transduce and encode, in general?

A

Noxious stimuli; eg:

  • Strong mechanical forces damaging tissue
  • Extremes in temperature
  • Chemical stimuli that damage skin like acid
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9
Q

What is a noxious stimulus encoded into by the nociceptor terminal?

A

Electrical signal

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10
Q

What is a noxious stimulus?

A

Stimulus that’s damaging/threatens damage to normal tissues

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11
Q

What are the three steps in transmission of nociception?

A

1) Action potential transfers electrical signal from periphery to spinal cord
2) Spinal cord nociceptive neurons integrate and transfer info to brains/other parts of spinal cord - 2nd neuron
3) Thalamic/brainstem nociceptive neurons integrate and transfer information to cortical and other brain regions

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12
Q

What are the two components of pain perception?

A

Sensory

Emotional

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13
Q

What does the sensory part of pain perception do?

A

Identifies discriminative aspects

  • Location
  • Intensity
  • Quality
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14
Q

What two ganglia contain primary afferent sensory neuron cell bodies?

A

Trigeminal ganglia

Dorsal root ganglia

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15
Q

What nociceptors do the trigeminal ganglia contain?

A

Those projecting to head

  • Migraine
  • Tooth and jaw pain
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16
Q

What nociceptors do the dorsal root ganglia contain?

A

Those projecting to body - most

  • Somatic
  • Visceral
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17
Q

How many axons does a nociceptive fibre have?

A

1 axon with 2 parts

  • Peripheral axon projecting via peripheral nerves to endings in somatic/visceral targets
  • Central axon projecting to dorsal horn of spinal cord
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18
Q

What are the types of nociceptive fibres?

A

C fibre

A delta fibre

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19
Q

Describe C fibres

A

Thin
Unmyelinated
Slow

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20
Q

Describe A delta fibres

A

Thin
Myelinated
Medium-fast

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21
Q

Compared to touch receptors, are nociceptive receptors fast or slow?

A

Slow

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22
Q

Describe the terminal of the peripheral axon of a nociceptive fibre

A

Free nerve endings

Not encapsulated in specialised cell like touch receptors

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23
Q

In which layers of the spinal cord do the central axons of nociceptors terminate?

A

Superficial layers - usually laminae 1 and 3

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24
Q

What is the nociceptive pathway in the spinal cord?

A

Those in dorsal horn project to brain via spinothalamic tract on opposite side of spinal cord

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25
Q

Where is the point of decussation in the nociceptive pathway?

A

Dorsal horn - via synapse

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26
Q

What white matter tract do nociceptors travel up in the spinal cord?

A

Anterolateral tract

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27
Q

Does all nociceptive information go up to the brain?

A

No, some only goes to spinal cord > forms reflex circuit

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28
Q

What happens when a noxious mechanical stimulus is detected by a nociceptor in the knee region?

A

Elicits complex withdrawal reflex in both legs without any input from brain

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29
Q

What happens to nociceptive information when the spinal cord is anaesthetised?

A

Perception of pain blocked because ascending pathway blocked

Spinal cord reflexes aren’t blocked

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30
Q

What type of pain do A delta fibres elicit?

A

Sharp

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31
Q

What type of pain do C fibres elicit?

A

Slow, burning

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32
Q

What type of behaviours are A delta fibres more likely to elicit?

A

Withdrawal reflex

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33
Q

What type of behaviours are C fibres more likely to elicit?

A

Behaviours that remove stimulus

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34
Q

Why can you feel a first and second pain?

A

When both A delta and C fibres are activated, they transmit signals at different speeds, so pain from A delta fibres is felt first, and quickly. Pain from C fibres follows and remains for a longer time

35
Q

What is inflammatory pain?

A

Pain felt during active inflammation

36
Q

How is inflammatory pain detected?

A

Properties of nociceptors altered by chemicals released by damaged tissues/immune system in context of disease

37
Q

What is spontaneous pain?

A

Pain felt when there is no external stimulus/pain with innocuous stimulus

38
Q

Why do we get spontaneous pain?

A

Sensory amplification

39
Q

Where can amplification happen?

A

Peripherally

Centrally

40
Q

What are clinically relevant stimuli for peripheral amplification?

A

Tissue trauma
Surgery
Joint inflammation; eg: rheumatoid arthritis

41
Q

What is one type transducer protein that’s found on nociceptors?

A

TRPV1

42
Q

What is TRPV1 activated by?

A

Capsaicin
Heat
Acid
Certain lipids - endogenous equivalents of cannabinoids

43
Q

Where is TRPV1 found?

A

Most membrane terminals of nociceptors?

44
Q

What type of receptor is TRPV1?

A

Gated ion channel for Na and Ca

45
Q

Do all nociceptors express the same transducer proteins?

A

No, different functional classes express different types

46
Q

What type of nociceptors is TRPV1 found on?

A

Polymodal nociceptors

Heat specialised nociceptors

47
Q

Do all members of the TRP respond to the same stimuli?

A

No, different members respond to different stimuli

48
Q

Where is TRPA1 found, and to what does it respond?

A 
In airways
Responds to
- Nicotine
- Formalin
- Others
49
Q

What does TRPM8 respond to?

A

Menthol

50
Q

How does the “inflammatory soup” affect nociceptor activity?

A

Chemical signals released by tissue damage/disease
Detected by different receptors on nociceptor terminals
Downstream cell signalling causes sensitisation

51
Q

How does downstream signalling affect nociceptor sensitisation?

A

Changes properties of terminal and lowers threshold

52
Q

Define hyperalgesia

A

Increased response to normally painful stimulus

53
Q

Define allodynia

A

Painful response to normally innocuous stimulus

54
Q

How can allodynia be clinically detected?

A

Stroke skin softly with paintbrush/cue tip > intensely painful to patient

55
Q

What can central sensitisation result from?

A

Increased nociceptor activity after peripheral sensitisation

56
Q

Describe secondary hyperalgesia

A

If you have localised painful stimulus, get localised pain induced by stimulus
Over time, hyperalgesia extends into areas that aren’t damaged because initial signal activates regions of spinal cord, including across segments
Amplifies info coming in from adjacent nociceptive and non-nociceptive afferent fibres

57
Q

What is neuropathic pain?

A

Nervous system lesion or disease/ marked neuroimmune response causing pain

58
Q

What are examples of a CNS problem causing neuropathic pain?

A

Stroke
Spinal cord injury
MS

59
Q

What causes central amplification in neuropathic pain?

A

Neuroimmune interactions in periphery and CNS

60
Q

What causes peripheral amplification in neuropathic pain?

A

Nerve trauma
Toxic and metabolic neuropathies
Herpes zoster
AIDS

61
Q

What does it mean for neuropathic pain to be maladaptive and persistent?

A

Abnormal amplification maintained independent of lesion/disease

62
Q

How can peripheral neuropatic pain occur?

A

Damage to peripheral nerves > develop inappropriate branches

Pain perception altered

63
Q

How can a cut terminal continue to produce spontaneous electrical activity?

A

Cell damage > nerve loses input > central part of axon continues to generate electrical activity

64
Q

What are complex regional pain syndromes (CRPS)?

A

Multifactorial pain disorder

  • Pain and other clinical abnormalities
    • Sensory
    • Motor
    • Autonomic
  • Signs and symptoms spread distally glove- or stocking-like in affected limbs
  • Sudden change for pain after fracture/surgery to persistent burning pain
65
Q

What is the cause of CRPS?

A

No identifiable pathology

66
Q

What are examples of functional pain syndromes?

A

CRPS
Migraines
Myalgia

67
Q

Define acute pain

A

Lasts for short time
Occurs after surgery/trauma/other condition
Warning to body to seek help

68
Q

Define sub-acute pain

A

Progressing to chronic pain
Can be prevented
Transition phase

69
Q

Define recurrent pain

A

Occurs on cyclical basis

  • Migraine
  • Pelvic pain
70
Q

Define chronic pain

A

Lasts beyond time expected for healing

71
Q

What area in the brain does pain activate?

A

No single area

Activates network

72
Q

What roles do the periaqueductal grey and rostral ventral medulla in the brainstem play in pain?

A

Form chain projecting back down to spinal cord

Modulate pain

73
Q

What are some major classes of centrally acting analgesic drugs?

A 
Opioids
NSAIDs
Anticonvulsants
Tricyclic antidepressants (TCAs)
Serotonin-noradrenaline reuptake inhibitors (SNRIs)
Alpha 2-adrenergic agonists
Cannabinoids
74
Q

What is an example of an opioid?

A

Morphine

75
Q

What are two examples of anticonvulsants?

A

Gabapentin

Pregabalin

76
Q

What is an example of an alpha 2-adrenergic agonist?

A

Clonidine

77
Q

What is an example of a cannabinoid?

A

Marijuana

78
Q

How can pain experience be modulated?

A

Feedback pathway to spinal cord that can inhibit/amplify info brought by nociceptors

79
Q

What effect does fear have on the perception of pain?

A

Hypoalgesia

80
Q

What cortical areas are involved in the modulation of pain?

A

Anterior cingulate
Prefrontal
Insula

81
Q

By giving a person a placebo and telling them that it reduces pain, what effect does this have in the brain?

A

Produces genuine analgesia via endogenous pain modulation

Placebo analgesia reduced/prevented by opioid antagonists

82
Q

What effect on the brain does it have by giving a patient a nocebo?

A

Hyperalgesia

83
Q

What are the factors in the psychobiological model of pain perception?

A 
A delta and C nociceptive input
Injury
- Peripheral and central sensitisation
Chemical and structure
- Neurodegeneration
- Metabolic
- Maladaptie plasticity
Cognitive set
- Hypervigilance
- Attention
- Distraction
- Catastrophising
Mood
- Depression
- Catastrophising
- Anxiety
Context
- Pain beliefs
- Expectation
- Placebo

MD1 Neuroscience (55 decks)

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