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Neuroscience > Pain > Flashcards

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
Q

What percent of neurons in the spinal cord have projections to the cervical level?

A

5-10% (1 in 9 neurons)

26
Q

What are interneurons?

A

make connections only within the spinal cord

27
Q

In what way does a painful stimulus not produce pain?

A

producing reflex responses (because perception of pain occurs in the brain)

28
Q

What is inflammatory pain?

A

produced by inflammatory mediators released in response to tissue damage eg macrophages, mast cells, neutrophils, granulocytes

29
Q

What threshold is nociceptive pain?

A

adaptive, high threshold pain - ie it acts as a warning system to be protective

30
Q

What threshold is inflammatory pain?

A

adaptive, low-threshold pain that is protective in promoting repair ie the tenderness you feel

31
Q

What are the features of inflammatory pain?

A

change in pain sensitivity; spontaneous pain (pain that is maintained continuously without stimulus/to normal stimulus/increased to the same painful stimulus)

32
Q

What comprises the inflammatory soup?

A

mixture of inflammatory mediators that signal tissue damage: macrophages, T lymphocytes, mast cells (bradykinin, histamine, PGE2), tissues releasing H+ or ATP

33
Q

How do nociceptors perceive inflammatory pain?

A

via receptors (GPCR, tyr kinase) or ion channels (eg capsaicin/TRPV1) activating signalling pathways in the nerve terminal

34
Q

What is the significance of TRP channels in nociception?

A

different types of pain-sensing nociceptors have different mixtures of TRP channels that determines what type of stimulus the nociceptor responds to

35
Q

TRPV1 responds to

A

heat (capsaicin receptor) 50-52 degrees - threshold is lowered in presence of capsaicin to physiological temperatures

36
Q

How does capsaicin (or H+) act at TRPV1?

A

activation opens the channel (maintained) and Ca2+ and Na+ ions enter the nerve terminal, depolarizing it creating electrical activity perceived as pain (heat)

37
Q

C fibres have which type of nociceptor channels?

A

polymodal: responding to heat and mechanical forces and chemicals - range of stimuli

38
Q

What do inflammatory chemicals do in terms of sensitization?

A

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
Q

Hyperalgesia

A

increased response to the same level of painful stimulation eg sunburn

40
Q

Allodynia

A

painful response to a normally innocuous stimulus (eg contacting clothes with a sunburn)

41
Q

How does central sensitization lead to secondary hyperalgesia?

A

central sensitization in the spinal cord expands the area of sensitivity beyond the region damaged - making the pain system more sensitive

42
Q

What are the two types of maladaptive pain?

A

Neuropathic and dysfunctional

43
Q

What is neuropathic pain?

A

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
Q

Neuropathic pain presents with which type of symptoms?

A

positive and negative

45
Q

Dysfunctional pain presents with which type of symptoms?

A

positive

46
Q

What is dysfunctional pain?

A

type of maladaptive pain; not associated with neural lesion, inflammation, pathology eg migraines, fibromyalgia, pelvic pain conditions

47
Q

What threshold is maladaptive pain?

A

maladaptive, low-threshold pain due to disease state of nervous system

48
Q

Maladaptive pain is

A

spontaneous and can produce hypersensitivity

49
Q

What is maladaptive pain?

A

spontaneous pain w/o stimulus, extreme allodynia, extrem hyperalgesia

50
Q

What brain regions are activated during pain?

A

PFC (higher order, emotion), anterior cingulate cortex (emotion), somatosensory cortex (sensorimotor)

51
Q

What are the affective components of pain?

A

emotional and motivational components of pain

52
Q

What components of pain become more important in chronic pain conditions (months-years)?

A

see a transition from sensory processing to emotional processing - emotional elements become more important

53
Q

What is the role of the periaqueductal grey pathway?

A

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
Q

What is the importance of the periaqueductal grey pathway?

A

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
Q

What is descending pain modulation?

A

spinal facilitation of pain from brain down the spinal cord eg engaged by inflammation - in the flu (to make you rest)

56
Q

Hypoalgesia

A

endogenous inhibition of pain sensitivity (analgesia)

57
Q

How is pain anticipation related to pain perception?

A

anxiety and fear (eg of pain) can produce hypoalgesia without actual physical stimulation

58
Q

What areas of the brain are involved in top-down psychological modulation of pain?

A

anterior cingulate cortex, PFC, insular cortex, amygdala (fear behaviour) - can be activated by drugs (via PAG) or fear to reduce pain sensitivity

59
Q

Why is the placebo effect considered not purely psychological?

A

can be blocked with an opioid antagonist

60
Q

What is the placebo effect?

A

use of a sugar pill produces genuine analgesia via endogenous pain modulation

61
Q

How do previous experience and learning alter pain?

A

producing positive (placebo) or negative (nocebo) expectations or beliefs

62
Q

What is the nocebo effect?

A

expectation of pain eg injections produces hyperalgesia

Neuroscience (15 decks)

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