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Peripheral and Central Pain > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

Three types of pain

A
  1. nociceptive
  2. neuropathic
  3. nociplastic
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2
Q

what is pain

A

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

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3
Q

adaptive role of pain

A

pain is a mainly protective mechanism for the body as it causes an individual to react and remove the pain stimulus

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4
Q

dimensions of pain

A
  1. sensory discriminative
  2. motivational affective
  3. cognitive evaluative
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5
Q

nociceptive pain

A

pain from a normal process that results in noxious stimuli being perceived as painful

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6
Q

neuropathic pain

A

pain that results as a direct consequence of a lesion or disease affecting abnormal functioning of the peripheral nervous system (PNS) or central nervous system (CNS)

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7
Q

nociplastic pain

A

pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain

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8
Q

three types of nociceptors

A

mechanical, thermal, chemical

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9
Q

thermal nociceptors

A

respond to temperature extremes, especially heat

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10
Q

mechanical nociceptors

A

Respond to mechanical damage such as cutting, crushing, or pinching

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11
Q

chemical nociceptors

A

selective responses to histamine and other chemicals

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12
Q

silent nociceptors

A

Pain receptors located within visceral organs that do not usually activate pain sensations by themselves but synapse onto the same 2nd order pain fibers in the spinal cord as peripheral nociceptors and facilitate the 2nd order neuron, causing increased sensitivity to peripheral stimuli.

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13
Q

polymodal nociceptors

A

respond to mechanical, thermal, and chemical stimuli

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14
Q

body regions without nociceptors

A

brain tissue, bone, interstitial tissue of the kidney, liver, and lungs

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15
Q

basic process of pain

A
  1. free nerve endings in tissues detect painful stimulus
  2. peripheral nerves send this signal
  3. reaches the dorsal horn of the spinal cord
  4. spinal cord pathway relays this information
  5. brain centers receive this information
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16
Q

free nerve endings

A

respond to pain and temperature

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17
Q

free nerve endings are nociceptors

A

due to the coating of ion channels that detect the presence of noxious stimuli

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18
Q

TRP Channels

A

transient receptor potential channels

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19
Q

transient receptor potential channels

A

painful heat or painful cold stimulates a whole different set of channels to open in the membrane called

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20
Q

TRPM8

A

cold sensor, menthol receptor

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21
Q

TRPV1

A

capsaicin receptor

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22
Q

mediator of capsaicin

A

TRPV1 mediates the pain-producing actions
- also activated by noxious heat stimuli
- suggests that it is normally transduces the sensation of painful heat

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23
Q

mishra et al., 2011

A

found that various strategies to eliminate TRPV1-expressing neurons in mice resulted in almost complete absence of heat nociception

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24
Q

caterina et al., 2000

A

In contrast to Mishra et al., genetic ablation of TRPV1 caused only minor deficits in acute noxious heat sensing

  • implying that heat‐sensitive nociceptors must express additional TRPV1‐independent heat‐sensing mechanisms.
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25
Q

vriens and voets (2019)

A

identified 3 TRP ion channels

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26
Q

vandewauw et al., 2018

A

The involvement of three heat sensing TRP channels with overlapping expression in nociceptor neurons represents a powerful mechanism that ensures avoidance of noxious heat, even under conditions where the function of one or two heat sensors is comprised

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27
Q

dorsal root ganglion

A

contains cell bodies of sensory neurons known as first-order neurons

28
Q

DRG axons

A

afferents that relay sensory information to the CNS

29
Q

A-beta fibres

A

large sensory fibers involved in rapidly transmitting sensation and possibly inhibiting the transmission of pain

30
Q

velocity of a-beta

A

30-70m/s

31
Q

diameter of a-beta

A

5-12um

32
Q

c-fibres

A

unmyelinated, slow-conducting fibers that carry peripheral impulses associated with pain to the spinal cord

33
Q

diameter of c-fibers

A

<0.4-1.2um

34
Q

velocity of c-fibers

A

0.5-2m/s

35
Q

c mechano-heat nociceptors

A

A tight linear relationship between pain and the level of noxious heat in human and monkey

36
Q

A-delta fibers

A

small-diameter nerve fibers that carry peripheral impulses associated with sharp initial pain to the spinal cord

37
Q

diameter of a-delta

A

2-5 microns

38
Q

velocity of a-delta

A

15-30m/s

39
Q

Two types of A delta fibers

A

type 1: slow response, long adaption

type 2: fast response, fast adaption

40
Q

fast sharp pain signals

A

elicited by mechanical or thermal pain stimuli

transmitted in peripheral nerves by small a-delta fibers

41
Q

slow-chronic pain signal

A

elicited by chemical types of pain stimuli

transmitted by c fibers

42
Q

double pain sensation

A

sensation that is caused by transmission of pain via TWO pathways in SPINAL THALAMIC TRACT.

43
Q

spinal cord

A

Nerves that run up and down the length of the back and transmit most messages between the body and brain

44
Q

lamina 1

A

lamina of the dorsal horn which receives A delta and C fibers

45
Q

lamina 2

A

substantia gelatinosa

46
Q

lamina 5

A

Proprioceptive, nociceptive, visceral input

47
Q

wide dynamic range neurons

A

receive input from nociceptive and non-nociceptive primary afferent fibers

48
Q

nociceptive-specific neurons

A
  • 2nd order neurons
  • serve only noxious stimuli
  • arranged somatotopically in lamina 1
  • have discrete (small), somatic receptive fields
  • normally silent
  • respond only to high-threshold noxious stimulation
  • poorly encode stimulus intensity
49
Q

wind up pain

A

heightened sensitivity that results in altered pain thresholds both peripherally and centrally

50
Q

temporal summation

A

A phenomenon of neural integration in which the membrane potential of the postsynaptic cell in a chemical synapse is determined by the combined effect of EPSPs or IPSPs produced in rapid succession.

51
Q

central sensitisation

A

Results from release of prostaglandins from nociceptive neurons. Consequences include non sensitive neurons may also become sensitised. Result of this is that normally innocuous stimuli can be perceived as painful.

52
Q

torebjork et al., 1992

A

This persistent, or regulated, state of reactivity lowers the threshold for what causes pain and subsequently comes to maintain pain even after the initial injury might have healed = SENSITISATION of the dorsal horn neuron

53
Q

two characteristics of central sensitization

A
  1. hyperalgesia
  2. allodynia
54
Q

hyperalgesia

A

increased pain sensitivity

55
Q

allodynia

A

pain due to stimulus that does not normally provoke pain

56
Q

glutamate

A

A major excitatory neurotransmitter

57
Q

substance p

A

A neurotransmitter that is involved in the transmission of pain messages to the brain.

58
Q

gaba

A

a major inhibitory neurotransmitter

59
Q

spinothalamic tract

A

nerve pathway from the spine to the thalamus along which pain impulses are carried to the brain

60
Q

3rd neuron

A

interneuron, axon reaches primary somatosensory cortex (postcentral gyrus)

61
Q

2nd neuron

A

post-ganglionic axon;
cell body located in autonomic ganglion; synapses with target cells / organ

62
Q

1st neuron

A

pre-ganglionic axon;
cell body located in spinal cord or brain

63
Q

gate control theory

A

melzak and wall (1965)

64
Q

melzak and wall (1965)

A

the theory that the spinal cord contains a neurological “gate” that blocks pain signals or allows them to pass on to the brain. The “gate” is opened by the activity of pain signals traveling up small nerve fibers and is closed by activity in larger fibers or by information coming from the brain.

65
Q

large myelinated fibers

A

strengthen the firing of SG interneurons via the colleterals of the dorsal column

= weak pain sensation due to the strong inhibition exerted by SG neurons

66
Q

small non-myelinated fibers

A

inhibit the activity of SG neurons and WDR neruons

= stronger pain sensation

67
Q

problems with gate control theory

A

Migraine headache often relieved by TENS to the temples; not anatomically related to spinal column, so no gating mechanism
GTC: must stimulate exact dermatome of pain
But electrodes several dermatome levels above or below pain site may relieve pain
So something other than gating must be acting to decrease pain
Pain may be reduced hours/days following TENS application not when gate should be active
Some born without pain perception ability, yet have abundance of nociceptors and neural circuits
Cannot account for phantom limb pain
Why specific stimulus evokes more or less pain over time?
How the placebo effect works?
Can’t explain how drugs moderating pain

Peripheral and Central Pain (1 decks)

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