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Pain Flashcards

1
Q

Nociceptive fibres are

A

C-fibres (slow, unmyelinated) and A-delta fibres (fast, myelinated)

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2
Q

C fibres and A-delta fibres detect

A

H+, heat, noxious cold, pressure, chemicals

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3
Q

What is different about nociceptors from other sensory fibres in peripheral tissues (eg mechano or thermoreceptors)?

A

they are only activated by strong forces that can actually damage tissues ie high levels of stimuli

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4
Q

What are the 4 stages involved in detecting a noxious stimuli?

A
  1. transduction
  2. transmission
  3. perception
  4. modulation
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5
Q

What happens in transduction of a noxious stimulus?

A

detection by the nociceptors creates an electrical event that transmits to the CNS (SC or brainstem)

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6
Q

What happens in transmission of a noxious stimulus?

A

transmission of information up to the brain (mostly thalamus) and then cortex

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7
Q

What happens in perception of a noxious stimulus?

A

transmitted information is perceived as pain only in the cortex - this is nociception

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8
Q

What happens in modulation of a noxious stimulus?

A

modulation occurs by interference of transmission or higher level perception of pain

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9
Q

What is nociceptive pain?

A

protective; induces a withdrawal reflex to prevent tissue damage

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10
Q

Nociceptors are activated by

A

high levels of heat, cold, intense mechanical forces, or chemical irritants; this distinguishes them from mechanoreceptors

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11
Q

Free endings of nociceptors are

A

unspecialized and free in tissues unlike mechanoreceptors which are enclosed in connective tissue

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12
Q

Cell bodies of somatosensory neurons are found in

A

dorsal root ganglia peripherally, cranial ganglia in the head (trigeminal)

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13
Q

C-fibres enter the spinal cord at

A

superficial layers in the grey matter dorsal horn: rexed laminae I and II

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14
Q

A-delta fibres enter the spinal cord at

A

superficial layers in the grey matter dorsal horn BUT project deeper down: rexed laminae I and V

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15
Q

Spinal DRG receive pain information from/to

A

somatic targets (skin, muscle, bone) and visceral targets (organs)

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16
Q

Trigeminal ganglia receive pain input from/to

A

tooth, jaw, migraine pain

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17
Q

Conduction by C-fibres takes

A

< 3m/s (about 1/3rd of a second to transmit to brain)

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18
Q

Conduction by A-delta fibres takes

A

10x faster than C-fibres; 3-30m/s (1/300th of a second to get to the brain)

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19
Q

What is glabrous skin?

A

hairless skin

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20
Q

A-delta fibres transmit which feeling of pain?

A

first/initial, sharp, very precisely localized type of pain

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21
Q

C-fibres transmit which feeling of pain?

A

later slow, burning, throbbing pain

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22
Q

Hairy skin (eg back of hands) has which type of pain fibres?

A

both: a-delta and C

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23
Q

Glabrous skin (eg palms/hairless) has which type of pain fibres?

A

only C fibres

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24
Q

Pain runs up the spinal cord in the

A

anterolateral/ventrolateral division of the spinal cord

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25
What percent of neurons in the spinal cord have projections to the cervical level?
5-10% (1 in 9 neurons)
26
What are interneurons?
make connections only within the spinal cord
27
In what way does a painful stimulus not produce pain?
producing reflex responses (because perception of pain occurs in the brain)
28
What is inflammatory pain?
produced by inflammatory mediators released in response to tissue damage eg macrophages, mast cells, neutrophils, granulocytes
29
What threshold is nociceptive pain?
adaptive, high threshold pain - ie it acts as a warning system to be protective
30
What threshold is inflammatory pain?
adaptive, low-threshold pain that is protective in promoting repair ie the tenderness you feel
31
What are the features of inflammatory pain?
change in pain sensitivity; spontaneous pain (pain that is maintained continuously without stimulus/to normal stimulus/increased to the same painful stimulus)
32
What comprises the inflammatory soup?
mixture of inflammatory mediators that signal tissue damage: macrophages, T lymphocytes, mast cells (bradykinin, histamine, PGE2), tissues releasing H+ or ATP
33
How do nociceptors perceive inflammatory pain?
via receptors (GPCR, tyr kinase) or ion channels (eg capsaicin/TRPV1) activating signalling pathways in the nerve terminal
34
What is the significance of TRP channels in nociception?
different types of pain-sensing nociceptors have different mixtures of TRP channels that determines what type of stimulus the nociceptor responds to
35
TRPV1 responds to
heat (capsaicin receptor) 50-52 degrees - threshold is lowered in presence of capsaicin to physiological temperatures
36
How does capsaicin (or H+) act at TRPV1?
activation opens the channel (maintained) and Ca2+ and Na+ ions enter the nerve terminal, depolarizing it creating electrical activity perceived as pain (heat)
37
C fibres have which type of nociceptor channels?
polymodal: responding to heat and mechanical forces and chemicals - range of stimuli
38
What do inflammatory chemicals do in terms of sensitization?
cause peripheral sensitization of nerve endings making them more sensitive to stimulation (primary allodynia/hyperalgesia); cause central sensitization making the pain system more sensitive (secondary allodynia/hyperalgesia)
39
Hyperalgesia
increased response to the same level of painful stimulation eg sunburn
40
Allodynia
painful response to a normally innocuous stimulus (eg contacting clothes with a sunburn)
41
How does central sensitization lead to secondary hyperalgesia?
central sensitization in the spinal cord expands the area of sensitivity beyond the region damaged - making the pain system more sensitive
42
What are the two types of maladaptive pain?
Neuropathic and dysfunctional
43
What is neuropathic pain?
type of maladaptive pain; involves damage to the nervous system (especially somatosensory) eg trauma, stroke, disease (MS) that increases sensitivity to stimuli (can fire w/o too)
44
Neuropathic pain presents with which type of symptoms?
positive and negative
45
Dysfunctional pain presents with which type of symptoms?
positive
46
What is dysfunctional pain?
type of maladaptive pain; not associated with neural lesion, inflammation, pathology eg migraines, fibromyalgia, pelvic pain conditions
47
What threshold is maladaptive pain?
maladaptive, low-threshold pain due to disease state of nervous system
48
Maladaptive pain is
spontaneous and can produce hypersensitivity
49
What is maladaptive pain?
spontaneous pain w/o stimulus, extreme allodynia, extrem hyperalgesia
50
What brain regions are activated during pain?
PFC (higher order, emotion), anterior cingulate cortex (emotion), somatosensory cortex (sensorimotor)
51
What are the affective components of pain?
emotional and motivational components of pain
52
What components of pain become more important in chronic pain conditions (months-years)?
see a transition from sensory processing to emotional processing - emotional elements become more important
53
What is the role of the periaqueductal grey pathway?
in pain, this pathway interferes with transmission from sensory terminals to projection neurons to higher centers in the brain; it relays through the ventral medulla then projects back to the dorsal horn of the spinal cord
54
What is the importance of the periaqueductal grey pathway?
most centrally-acting analgesic or pain relieving drugs activate this pathway to block transfer of pain information - opioids, NSAIDs, anticonvulsants, cannabinoids, a2-adrenergic agonists, TCAs and other antidepressants like SNRIs
55
What is descending pain modulation?
spinal facilitation of pain from brain down the spinal cord eg engaged by inflammation - in the flu (to make you rest)
56
Hypoalgesia
endogenous inhibition of pain sensitivity (analgesia)
57
How is pain anticipation related to pain perception?
anxiety and fear (eg of pain) can produce hypoalgesia without actual physical stimulation
58
What areas of the brain are involved in top-down psychological modulation of pain?
anterior cingulate cortex, PFC, insular cortex, amygdala (fear behaviour) - can be activated by drugs (via PAG) or fear to reduce pain sensitivity
59
Why is the placebo effect considered not purely psychological?
can be blocked with an opioid antagonist
60
What is the placebo effect?
use of a sugar pill produces genuine analgesia via endogenous pain modulation
61
How do previous experience and learning alter pain?
producing positive (placebo) or negative (nocebo) expectations or beliefs
62
What is the nocebo effect?
expectation of pain eg injections produces hyperalgesia

Neuroscience (15 decks)

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